Journal articles: 'Metastasis promotion'

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Kitamura, Takanori, Bin-Zhi Qian, and Jeffrey W. Pollard. "Immune cell promotion of metastasis." Nature Reviews Immunology 15, no. 2 (January 23, 2015): 73–86. http://dx.doi.org/10.1038/nri3789.

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Mathias, Alissa B., Eric P. Palmer, Nicole Kruh-Garcia, and Daniel P. Regan. "The role of osteosarcoma cell-derived exosomes in the promotion of lung metastasis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 242.44. http://dx.doi.org/10.4049/jimmunol.204.supp.242.44.

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Abstract Osteosarcoma (OS) is the most common primary tumor of bone and typically occurs in children and young adults. 30–40% of OS patients develop lung metastases after initial diagnosis, with only 20% of these patients surviving 4 years post-relapse. For over 30 years, there have been no improvements in the treatment of OS, and more importantly, no diagnostic tools that help identify those patients at high risk for lung metastases. Recent data has shown that in other tumor types, tumor-secreted extracellular vesicles (EVs) deliver biological cargo to distant sites, resulting in priming of non-malignant host cells for promotion of metastasis. The aim of this project is to understand how OS EVs influence the response of lung fibroblasts (LFs) and alveolar macrophages (AMs), and if their uptake of EVs results in pre-metastatic priming that can be detected via AM transcriptomic changes. Hypothesis LFs are primary targets of OS EVs, which will increase LF IL-6 production and cause paracrine STAT3 activation of AM’s into an M2 tumor-promoting phenotype. Results Flow cytometry and confocal microscopy demonstrated in vitro uptake of OS EVs by LF cells. In vitro ‘education’ of LFs with OS EVs induced significant production of IL-6, IL-8, and CCL2, with the greatest mean difference between EV-educated and naïve LFs observed with IL-6 secretion. Conclusion This data suggest that OS EVs efficiently prime LFs to induce IL-6 secretion, and this response may be associated with promotion of OS lung metastasis. Further data is being collected to determine the role of IL-6 in OS cell survival and lung metastatic colonization. RNA sequencing of AMs will be used to characterize phenotype which could serve as an effective cellular biomarker to predict lung metastasis.

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Solinas, Graziella, Federica Marchesi, Cecilia Garlanda, Alberto Mantovani, and Paola Allavena. "Inflammation-mediated promotion of invasion and metastasis." Cancer and Metastasis Reviews 29, no. 2 (April 24, 2010): 243–48. http://dx.doi.org/10.1007/s10555-010-9227-2.

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Lin, Richard J., Vahid Afshar-Kharghan, and Andrew I. Schafer. "Paraneoplastic thrombocytosis: the secrets of tumor self-promotion." Blood 124, no. 2 (July 10, 2014): 184–87. http://dx.doi.org/10.1182/blood-2014-03-562538.

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Abstract Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival. Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation. Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis. Taken together, these findings provide exciting new potential targets for therapeutic intervention.

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Bar-Yosef, Shahar, Rivka Melamed, Gayle G. Page, Guy Shakhar, Keren Shakhar, and Shamgar Ben-Eliyahu. "Attenuation of the Tumor-promoting Effect of Surgery by Spinal Blockade in Rats." Anesthesiology 94, no. 6 (June 1, 2001): 1066–73. http://dx.doi.org/10.1097/00000542-200106000-00022.

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Background The perioperative period is characterized by a state of immunosuppression, which was shown in animal studies to underlie the promotion of tumor metastasis by surgery. As this immunosuppression is partly ascribed to the neuroendocrine stress response, the authors hypothesized that spinal blockade, known to attenuate this response, may reduce the tumor-promoting effect of surgery. Methods Fischer-344 rats were subjected to a laparotomy during general halothane anesthesia alone or combined with either systemic morphine (10 mg/kg) or spinal block using bupivacaine (50 microg) with morphine (10 microg). Control groups were either anesthetized or undisturbed. Blood was drawn 5 h after surgery to assess number and activity of natural killer cells, or rats were inoculated intravenously with MADB106 adenocarcinoma cells, which metastasize only to the lungs. Metastatic development was assessed by quantifying lung retention of tumor cells 24 h after inoculation or by counting pulmonary metastases 3 weeks later. Results Laparotomy conducted during general anesthesia alone increased lung tumor retention up to 17-fold. The addition of spinal block reduced this effect by 70%. The number of metastases increased from 16.7 +/- 10.5 (mean +/- SD) in the control group to 37.2 +/- 24.4 after surgery and was reduced to 10.5 +/- 4.7 during spinal block. Systemic morphine also reduced the effects of surgery, but to a lesser degree. Natural killer cell activity was suppressed to a similar extent by surgery and by anesthesia alone. Conclusions The addition of spinal blockade to general halothane anesthesia markedly attenuates the promotion of metastasis by surgery.

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Reticker-Flynn, Nathan E., Weiruo Zhang, Julia A. Belk, Pamela A. Basto, Andrew J. Gentles, John B. Sunwoo, Ansuman K. Satpathy, Sylvia K. Plevritis, and Edgar G. Engleman. "Abstract PR013: Lymph node colonization promotes distant tumor metastasis through the induction of tumor-specific immune tolerance." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): PR013. http://dx.doi.org/10.1158/1538-7445.metastasis22-pr013.

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Abstract The majority of cancer-associated deaths result from distant organ metastasis, yet the mechanisms that enable this process remain poorly understood. For most solid tumors, colonization of regional or distant lymph nodes (LNs) typically precedes the formation of distant organ metastases, yet it remains unclear whether LN metastasis plays a functional role in disease progression. LNs are major sites of anti-tumor lymphocyte education, including in the context of immunotherapy, yet LN metastasis frequently correlates with further disease progression. Here, we find that LN metastasis represents a critical step in tumor progression through the capacity of such metastases to induce tumor-specific immune tolerance in a manner that promotes further dissemination of tumors to distant organs. Using an in vivo passaging approach of a non-metastatic syngeneic melanoma, we generated 300 unique cell lines exhibiting varying degrees of LN metastatic capacity. We show that the presence of these LN metastases enables distant organ seeding of metastases in a manner that the parental tumor cannot, and this effect is eliminated in mice lacking an adaptive immune response. Furthermore, this promotion of distant seeding by LN metastases is tumor specific. Using flow cytometry and single-cell sequencing to perform comprehensive immune profiling, we identify multiple cellular mediators of tolerance. In particular, we find that LN metastases have the capacity to both resist NK cell cytotoxicity and induce regulatory T cells (Tregs). Furthermore, depletion of NK cells in vivo enables non-metastatic tumors to disseminate to LNs, and ablation of Tregs using FoxP3-DTR mice eliminates the occurrence of lymphatic metastases. Adoptive transfer of Tregs from the LNs of mice bearing LN metastasis to naïve mice facilitates metastasis in a manner that Tregs from mice without LN metastases cannot, and we find that these Tregs are induced in an antigen-specific manner. Whole exome sequencing revealed that neither the metastatic proclivity nor immunosuppression evolve through the acquisition of driver mutations, loss of neoantigens, loss of MHC class I presentation, or decreases in melanoma antigen expression. Rather, by RNA-seq and ATAC-seq, we show that a conserved interferon signaling axis is upregulated in LN metastases and is rendered stable through epigenetic reprogramming of chromatin accessibility resulting from chronic exposure to interferons in vivo. Furthermore, using CRISPR/Cas9, we find that these pathways are required for LN metastatic seeding, and validate their conserved significance in additional mouse models of pancreatic ductal adenocarcinoma and head and neck squamous cell carcinoma and humans with LN metastatic disease. Together, these findings demonstrate a critical role for LN metastasis in promoting tumor-specific immunosuppression. Citation Format: Nathan E. Reticker-Flynn, Weiruo Zhang, Julia A. Belk, Pamela A. Basto, Andrew J. Gentles, John B. Sunwoo, Ansuman K. Satpathy, Sylvia K. Plevritis, Edgar G. Engleman. Lymph node colonization promotes distant tumor metastasis through the induction of tumor-specific immune tolerance [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr PR013.

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Hirakawa, Satoshi, Lawrence F. Brown, Shohta Kodama, Karri Paavonen, Kari Alitalo, and Michael Detmar. "VEGF-C–induced lymphangiogenesis in sentinel lymph nodes promotes tumor metastasis to distant sites." Blood 109, no. 3 (October 10, 2006): 1010–17. http://dx.doi.org/10.1182/blood-2006-05-021758.

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Abstract The mechanisms by which tumors metastasize to sentinel and distant lymph nodes, and beyond, are poorly understood. We developed transgenic mice that overexpress vascular endothelial growth factor-C (VEGF-C) and green fluorescent protein specifically in the skin and studied the effects of chemically-induced skin carcinogenesis in this model. We found that in contrast to VEGF-A, VEGF-C does not increase the growth of primary tumors, but instead induces expansion of lymphatic networks within sentinel lymph nodes, even before the onset of metastasis. Once the metastatic cells arrived at the sentinel lymph nodes, the extent of lymphangiogenesis at these sites increased. Of importance, in mice with metastasis-containing sentinel lymph nodes, tumors that expressed VEGF-C were more likely to metastasize to additional organs, such as distal lymph nodes and lungs. No metastases were observed in distant organs in the absence of lymph node metastases. These findings indicate an important role of VEGF-C–induced lymph node lymphangiogenesis in the promotion of cancer metastasis beyond the sentinel lymph nodes. VEGF-C is therefore a good target to slow or even prevent the onset of metastasis.

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Wei, Qinyao, Yun Qian, Jun Yu, and Chi Chun Wong. "Metabolic rewiring in the promotion of cancer metastasis: mechanisms and therapeutic implications." Oncogene 39, no. 39 (August 24, 2020): 6139–56. http://dx.doi.org/10.1038/s41388-020-01432-7.

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Abstract Tumor metastasis is the major cause of mortality from cancer. Metabolic rewiring and the metastatic cascade are highly intertwined, co-operating to promote multiple steps of cancer metastasis. Metabolites generated by cancer cells influence the metastatic cascade, encompassing epithelial-mesenchymal transition (EMT), survival of cancer cells in circulation, and metastatic colonization at distant sites. A variety of molecular mechanisms underlie the prometastatic effect of tumor-derived metabolites, such as epigenetic deregulation, induction of matrix metalloproteinases (MMPs), promotion of cancer stemness, and alleviation of oxidative stress. Conversely, metastatic signaling regulates expression and activity of rate-limiting metabolic enzymes to generate prometastatic metabolites thereby reinforcing the metastasis cascade. Understanding the complex interplay between metabolism and metastasis could unravel novel molecular targets, whose intervention could lead to improvements in the treatment of cancer. In this review, we summarized the recent discoveries involving metabolism and tumor metastasis, and emphasized the promising molecular targets, with an update on the development of small molecule or biologic inhibitors against these aberrant situations in cancer.

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Erpenbeck, Luise, Bernhard Nieswandt, Margarete Schön, Miroslava Pozgajova, and Michael P. Schön. "Inhibition of Platelet GPIbα and Promotion of Melanoma Metastasis." Journal of Investigative Dermatology 130, no. 2 (February 2010): 576–86. http://dx.doi.org/10.1038/jid.2009.278.

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Orosz, Peter, Achim Krüger, Marcus Hubbe, Josef Rüschoff, Paul Von Hoegen, and Daniela N. Männel. "Promotion of experimental liver metastasis by tumor necrosis factor." International Journal of Cancer 60, no. 6 (March 16, 1995): 867–71. http://dx.doi.org/10.1002/ijc.2910600624.

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Sharma, Rajesh, Zinal Chheda, Venkatakrishna Jala, Shuchismita Satpathy, and Bodduluri Haribabu. "Role and association of CD11b and Gr1+ cells in promotion of spontaneous lung cancer metastasis (TUM4P.920)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 138.21. http://dx.doi.org/10.4049/jimmunol.192.supp.138.21.

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Abstract Microenvironment plays an important role in tumor growth and metastasis. We established a unique metastasis model by in vivo passaging the Lewis lung carcinoma (3LL) cells with 7-11 days of culture in between passages. When injected subcutaneously the parental (3LL) cells have minimal metastasis whereas the in vivo passaged (p3LL) cells showed robust metastasis. The goal of this study is to identify the immune population that enhances the metastatic propensity of tumor cells. Purified p3LL (CD45-) cells also yielded similar metastasis excluding a direct role of residual immune cells in promotion of metastasis. The p3LL cells metastasized at similar frequency in WT and Rag2-/- mice indicating that adaptive immune cells are not required for metastasis. Analysis of tumors derived from 3LL vs p3LL revealed differential accumulation of CD11b+Gr1+ subpopulations. 3LL tumors contained higher CD11b+ Gr1high cells whereas p3LL tumors showed higher levels of CD11b+ Gr1low population. Interestingly, when CD11b+ Gr1low populations were isolated from spleen of p3LL tumor bearing mice and co-cultured with 3LL cells for 5 days, these cells acquired enhanced metastatic capacity as compared to control 3LL cells. These results indicate a distinct association and a critical role of CD11b+ Gr1low population in promotion of metastatic phenotype and suggest that abundance of CD11b+ Gr1low population may serve as a marker and a potential therapeutic target for inhibiting Lung cancer metastasis.

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D’Alterio, Crescenzo, Stefania Scala, Gabriella Sozzi, Luca Roz, and Giulia Bertolini. "Paradoxical effects of chemotherapy on tumor relapse and metastasis promotion." Seminars in Cancer Biology 60 (February 2020): 351–61. http://dx.doi.org/10.1016/j.semcancer.2019.08.019.

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Liu, Daren, Chao Li, Bogusz Trojanowicz, Xiaowen Li, Dike Shi, Chenni Zhan, Zhefang Wang, and Li Chen. "CD97 promotion of gastric carcinoma lymphatic metastasis is exosome dependent." Gastric Cancer 19, no. 3 (August 2, 2015): 754–66. http://dx.doi.org/10.1007/s10120-015-0523-y.

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Rysz, Jacek, Tomasz Konecki, Beata Franczyk, Janusz Ławiński, and Anna Gluba-Brzózka. "The Role of Long Noncoding RNA (lncRNAs) Biomarkers in Renal Cell Carcinoma." International Journal of Molecular Sciences 24, no. 1 (December 30, 2022): 643. http://dx.doi.org/10.3390/ijms24010643.

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Renal cell carcinoma is one of the common cancers whose incidence and mortality are continuously growing worldwide. Initially, this type of tumour is usually asymptomatic. Due to the lack of reliable diagnostic markers, one-third of ccRCC patients already have distant metastases at the time of diagnosis. This underlines the importance of establishing biomarkers that would enable the prediction of the disease’s course and the risk of metastasis. LncRNA, which modulates genes at the epigenetic, transcriptional, and post-transcriptional levels, appears promising. The actions of lncRNA involve sponging and sequestering target miRNAs, thus affecting numerous biological processes. Studies have confirmed the involvement of RNAs in various diseases, including RCC. In this review, we focused on MALAT1 (a marker of serious pathological changes and a factor in the promotion of tumorigenesis), RCAT1 (tumour promoter in RCC), DUXAP9 (a plausible marker of localized ccRCC), TCL6 (exerting tumour-suppressive effects in renal cancer), LINC00342 (acting as an oncogene), AGAP2 Antisense1 (plausible predictor of RCC progression), DLEU2 (factor promoting tumours growth via the regulation of epithelial-mesenchymal transition), NNT-AS1 (sponge of miR-22 contributing to tumour progression), LINC00460 (favouring ccRCC development and progression) and Lnc-LSG1 (a factor that may stimulate ccRCC metastasis).

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Evans, Caroline, and Bernard Corfe. "Promotion of cancer metastasis: candidate validation using an iTRAQ-based approach." Expert Review of Proteomics 10, no. 4 (August 2013): 321–23. http://dx.doi.org/10.1586/14789450.2013.820538.

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Park, Joon Seong, Ji-hae Lee, Yun Sun Lee, Jae Keun Kim, Seung Myung Dong, and Dong Sup Yoon. "Emerging role of LOXL2 in the promotion of pancreas cancer metastasis." Oncotarget 7, no. 27 (June 7, 2016): 42539–52. http://dx.doi.org/10.18632/oncotarget.9918.

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Browning, Landon, Megha Patel, Eli Bring Horvath, Ken Tawara, and Cheryl L. Jorcyk. "IL-6 and ovarian cancer: inflammatory cytokines in promotion of metastasis." Cancer Management and Research Volume 10 (December 2018): 6685–93. http://dx.doi.org/10.2147/cmar.s179189.

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Chen, Xin, Qingyong Ma, and Zheng Wu. "Arl4C-mediate promotion in the growth and metastasis of pancreatic cancer." Pancreatology 16, no. 1 (January 2016): S37. http://dx.doi.org/10.1016/j.pan.2015.12.113.

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McKenzie, Jodi A., Tong Liu, Jae Y. Jung, Benjamin B. Jones, Huseyin A. Ekiz, Alana L. Welm, and Douglas Grossman. "Survivin promotion of melanoma metastasis requires upregulation of α 5 integrin." Carcinogenesis 34, no. 9 (May 2, 2013): 2137–44. http://dx.doi.org/10.1093/carcin/bgt155.

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Avnet, Sofia, Silvia Lemma, Margherita Cortini, Gemma Di Pompo, Francesca Perut, Maria Veronica Lipreri, Laura Roncuzzi, et al. "The Release of Inflammatory Mediators from Acid-Stimulated Mesenchymal Stromal Cells Favours Tumour Invasiveness and Metastasis in Osteosarcoma." Cancers 13, no. 22 (November 22, 2021): 5855. http://dx.doi.org/10.3390/cancers13225855.

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Osteosarcoma is the most frequent primary malignant bone tumour with an impressive tendency to metastasise. Highly proliferative tumour cells release a remarkable amount of protons into the extracellular space that activates the NF-kB inflammatory pathway in adjacent stromal cells. In this study, we further validated the correlation between tumour glycolysis/acidosis and its role in metastases. In patients, at diagnosis, we found high circulating levels of inflammatory mediators (IL6, IL8 and miR-136-5p-containing extracellular vesicles). IL6 serum levels significantly correlated with disease-free survival and 18F-FDG PET/CT uptake, an indirect measurement of tumour glycolysis and, hence, of acidosis. In vivo subcutaneous and orthotopic models, co-injected with mesenchymal stromal (MSC) and osteosarcoma cells, formed an acidic tumour microenvironment (mean pH 6.86, as assessed by in vivo MRI-CEST pH imaging). In these xenografts, we enlightened the expression of both IL6 and the NF-kB complex subunit in stromal cells infiltrating the tumour acidic area. The co-injection with MSC also significantly increased lung metastases. Finally, by using 3D microfluidic models, we directly showed the promotion of osteosarcoma invasiveness by acidosis via IL6 and MSC. In conclusion, osteosarcoma-associated MSC react to intratumoural acidosis by triggering an inflammatory response that, in turn, promotes tumour invasiveness at the primary site toward metastasis development.

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Varga, Attila, Minh Tu Nguyen, Kinga Pénzes, Bence Bátai, Pál Gyulavári, Bianka Gurbi, József Murányi, et al. "Protein Kinase D3 (PKD3) Requires Hsp90 for Stability and Promotion of Prostate Cancer Cell Migration." Cells 12, no. 2 (January 4, 2023): 212. http://dx.doi.org/10.3390/cells12020212.

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Prostate cancer metastasis is a significant cause of mortality in men. PKD3 facilitates tumor growth and metastasis, however, its regulation is largely unclear. The Hsp90 chaperone stabilizes an array of signaling client proteins, thus is an enabler of the malignant phenotype. Here, using different prostate cancer cell lines, we report that Hsp90 ensures PKD3 conformational stability and function to promote cancer cell migration. We found that pharmacological inhibition of either PKDs or Hsp90 dose-dependently abrogated the migration of DU145 and PC3 metastatic prostate cancer cells. Hsp90 inhibition by ganetespib caused a dose-dependent depletion of PKD2, PKD3, and Akt, which are all involved in metastasis formation. Proximity ligation assay and immunoprecipitation experiments demonstrated a physical interaction between Hsp90 and PKD3. Inhibition of the chaperone–client interaction induced misfolding and proteasomal degradation of PKD3. PKD3 siRNA combined with ganetespib treatment demonstrated a specific involvement of PKD3 in DU145 and PC3 cell migration, which was entirely dependent on Hsp90. Finally, ectopic expression of PKD3 enhanced migration of non-metastatic LNCaP cells in an Hsp90-dependent manner. Altogether, our findings identify PKD3 as an Hsp90 client and uncover a potential mechanism of Hsp90 in prostate cancer metastasis. The molecular interaction revealed here may regulate other biological and pathological functions.

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Sabol, Rachel A., Adam Beighley, Paulina Giacomelli, Rachel M. Wise, Mark A. A. Harrison, Ben A. O’Donnnell, Brianne N. Sullivan, et al. "Obesity-Altered Adipose Stem Cells Promote ER+ Breast Cancer Metastasis through Estrogen Independent Pathways." International Journal of Molecular Sciences 20, no. 6 (March 20, 2019): 1419. http://dx.doi.org/10.3390/ijms20061419.

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Adipose stem cells (ASCs) play an essential role in tumor microenvironments. These cells are altered by obesity (obASCs) and previous studies have shown that obASCs secrete higher levels of leptin. Increased leptin, which upregulates estrogen receptor alpha (ERα) and aromatase, enhances estrogen bioavailability and signaling in estrogen receptor positive (ER+) breast cancer (BC) tumor growth and metastasis. In this study, we evaluate the effect of obASCs on ER+BC outside of the ERα signaling axis using breast cancer models with constitutively active ERα resulting from clinically relevant mutations (Y537S and D538G). We found that while obASCs promote tumor growth and proliferation, it occurs mostly through abrogated estrogen signaling when BC has constitutive ER activity. However, obASCs have a similar promotion of metastasis irrespective of ER status, demonstrating that obASC promotion of metastasis may not be completely estrogen dependent. We found that obASCs upregulate two genes in both ER wild type (WT) and ER mutant (MUT) BC: SERPINE1 and ABCB1. This study demonstrates that obASCs promote metastasis in ER WT and MUT xenografts and an ER MUT patient derived xenograft (PDX) model. However, obASCs promote tumor growth only in ER WT xenografts.

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Li, Dawei, Ping Wei, Zhihai Peng, Chen Huang, Huamei Tang, Zhiliang Jia, Jiujie Cui, Xiangdong Le, Suyun Huang, and Keping Xie. "The critical role of dysregulated FOXM1–PLAUR signaling in human colon cancer progression and metastasis." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 405. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.405.

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405 Background: The mammalian Forkhead Box (Fox) transcription factor FOXM1 is implicated in tumorigenesis including mouse intestinal cancer. However, the clinical significance of FOXM1 signaling in human colorectal cancer (CRC) pathogenesis remains unknown. Methods: We investigated FOXM1 expression in 203 cases of primary colon cancer and matched normal colon tissue specimens and explored the underlying mechanisms of altered FOXM1 expression and the impact of this altered expression on colon cancer growth and metastasis using in vitro and animal models of colon cancer. Results: We found weak expression of FOXM1 protein in the colon mucosa, whereas we observed strong FOXM1 expression in tumor-cell nuclei of colon cancer and lymph node metastases. A Cox proportional hazards model revealed that FOXM1 expression was an independent prognostic factor in multivariate analysis. Experimentally, overexpression of FOXM1 by gene transfer significantly promoted the growth and metastasis of colon cancer cells in orthotopic mouse models, whereas knockdown of FOXM1 expression by small interfering RNA did the opposite. Promotion of colon tumorigenesis by FOXM1 directly and significantly correlated with activation of urokinase plasminogen activator receptor (PLAUR) expression and elevation of invasion and metastasis. Conclusions: Given the importance of FOXM1 in regulation of the expression of genes key to cancer biology, dysregulated expression and activation of FOXM1 may play important roles in colon cancer progression and metastasis.

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Li, Cong, Xia Wu, Wei Zhang, Jia Li, Huawei Liu, Ming Hao, Junsong Wang, et al. "High-Content Functional Screening of AEG-1 and AKR1C2 for the Promotion of Metastasis in Liver Cancer." Journal of Biomolecular Screening 21, no. 1 (August 28, 2015): 101–7. http://dx.doi.org/10.1177/1087057115603310.

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Liver cancer is one of the most lethal cancer types in humans, but our understanding of the molecular mechanisms underlying this process remains insufficient. Here, we conducted high-content screening of the potential genes involved in liver cancer metastasis, which we selected from the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database, based on the SAMcell method and RNA interference technology. We identified two powerful genes in the liver cancer metastasis process, AEG-1 and AKR1C2, both of which proved to be positive regulators in promoting metastasis in liver cancer. Further clinical results verified their roles in liver cancer. In summary, these findings could provide new insight into the liver cancer mechanism and potentially therapeutic novel targets for liver cancer therapies in the future.

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Su, Yaowu, Liang Zhou, Qin Yu, Jianjun Lu, and Wei Liu. "Long Non-Coding RNA LOC648987 Promotes Proliferation and Metastasis of Renal Cell Carcinoma by Regulating Epithelial-Mesenchymal Transition." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382199783. http://dx.doi.org/10.1177/1533033821997834.

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Renal cell carcinoma (RCC) is a type of urinary tumor with a high incidence and is often associated with tumor metastasis. Long non-coding RNA (lncRNA) regulates tumorigenesis, progression, and metastasis. However, the role and the predictive value of lncRNA in RCC progression and metastasis have not been elucidated. The purpose of this study was to evaluate the effect of a newly discovered lncRNA LOC648987 on RCC proliferation and metastasis. LOC648987 was identified by RT-PCR for high expression in human RCC tissues as well as in metastatic RCC tissues. In the cell experiments, we infected the RCC cell lines ACHN and 786-O cells with LOC648987-shRNA and its negative control (shNC). The results showed that the knockdown of LOC648987 inhibited the proliferation of ACHN and 786-O cells and colony formation. The cell cycle and the apoptosis progression of ACHN and 786-O cells were assessed using flow cytometry. The knockdown of LOC648987 significantly inhibited the progression of ACHN and 786-O cells from G0/G1 to S phase and promoted cell apoptosis. The metastasis promoting effects of LOC648987 on ACHN and 786-O cells were verified by transwell migration assays, which depended on vimentin and MMP-9 to regulate the epithelial–mesenchymal transition. Finally, the promotion of LOC648987 on RCC tumorigenesis was evaluated in BALb/c nude mice. These data confirmed that lncRNA LOC648987 promoted RCC cell proliferation and tumor metastasis and regulated the expression of EMT-related proteins in RCC cells.

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Hu, Sike, Xiaoli Dong, Wenjuan Gao, Dwayne Stupack, Yanhua Liu, Rong Xiang, and Na Li. "Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation." Oncotarget 8, no. 34 (April 28, 2017): 56569–81. http://dx.doi.org/10.18632/oncotarget.17507.

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Tu, Dom-Gene, Wen-Wei Chang, Ming-Shiou Jan, Chi-Wen Tu, Yin-Che Lu, and Chien-Kuo Tai. "Promotion of metastasis of thyroid cancer cells via NRP-2-mediated induction." Oncology Letters 12, no. 5 (September 20, 2016): 4224–30. http://dx.doi.org/10.3892/ol.2016.5153.

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Luo, Weixin, Shusheng Lin, Yipei Huang, Ke Zhu, Fapeng Zhang, Junlong Lin, Yufei Qin, Ziyu Zhou, Wenrui Wu, and Chao Liu. "Bioinformatic Analysis and In Vitro and In Vivo Experiments Reveal That Fibrillarin Participates in the Promotion of Lung Metastasis in Hepatocellular Carcinoma." Bioengineering 9, no. 8 (August 17, 2022): 396. http://dx.doi.org/10.3390/bioengineering9080396.

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Lung metastasis, the most frequent metastatic pattern in hepatocellular carcinoma, is an important contributor to poor prognosis. However, the mechanisms responsible for lung metastasis in hepatocellular carcinoma remain unknown. Aiming to explore these mechanisms, weighted gene coexpression network analysis (WGCNA) was firstly used to find hub genes related to lung metastasis. Then, we obtained 67 genes related to lung metastasis in hepatocellular carcinoma which were mainly related to ribosomal pathways and functions, and a protein interaction network analysis identified that fibrillarin (FBL) might be an important hub gene. Furthermore, we found that FBL is highly expressed in hepatocellular carcinoma and that its high expression increases the rate of lung metastasis and indicates a poor prognosis. Knockdown of FBL could significantly reduce proliferation and stemness as well as inhibiting the migration and invasion of hepatocellular carcinoma cells. Moreover, we found that FBL might be involved in the regulation of MYC and E2F pathways in hepatocellular carcinoma. Finally, we demonstrated that the knockdown of FBL could suppress hepatocellular carcinoma cell growth in vivo. In conclusion, ribosome-biogenesis-related proteins, especially Fibrillarin, play important roles in lung metastasis from hepatocellular carcinoma.

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Gordon-Weeks, Alex, Su Yin Lim, Arseniy Yuzhalin, Serena Lucotti, Jenny Adriana Francisca Vermeer, Keaton Jones, Jianzhou Chen, and Ruth J. Muschel. "Tumour-Derived Laminin α5 (LAMA5) Promotes Colorectal Liver Metastasis Growth, Branching Angiogenesis and Notch Pathway Inhibition." Cancers 11, no. 5 (May 6, 2019): 630. http://dx.doi.org/10.3390/cancers11050630.

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Hepatic metastatic growth is dependent upon stromal factors including the matrisomal proteins that make up the extracellular matrix (ECM). Laminins are ECM glycoproteins with several functions relevant to tumour progression including angiogenesis. We investigated whether metastatic colon cancer cells produce the laminins required for vascular basement membrane assembly as a mechanism for the promotion of angiogenesis and liver metastasis growth. qPCR was performed using human-specific primers to laminin chains on RNA from orthotopic human colorectal liver metastases. Laminin α5 (LAMA5) expression was inhibited in colon cancer cells using shRNA. Notch pathway gene expression was determined in endothelia from hepatic metastases. Orthotopic hepatic metastases expressed human laminin chains α5, β1 and γ1 (laminin 511), all of which are required for vascular basement membrane assembly. The expression of Laminin 511 was associated with reduced survival in several independent colorectal cancer cohorts and angiogenesis signatures or vessel density significantly correlated with LAMA5 expression. Colorectal cancer cells in culture made little LAMA5, but its levels were increased by culture in a medium conditioned by tumour-derived CD11b+ myeloid cells through TNFα/NFκB pathway signalling. Down-regulation of LAMA5 in cancer cells impaired liver metastatic growth and resulted in reduced intra-tumoural vessel branching and increased the expression of Notch pathway genes in metastasis-derived endothelia. This data demonstrates a mechanism whereby tumour inflammation induces LAMA5 expression in colorectal cancer cells. LAMA5 is required for the successful growth of hepatic metastases where it promotes branching angiogenesis and modulates Notch signalling.

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Wang, Haihong, Zhenyu Lin, Tao Zhang, and Jinghua Ren. "Relationship of KIAA1199 on neutrophil recruitment and promotion of colorectal cancer liver metastasis via TGF-β signaling." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16005-e16005. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16005.

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e16005 Background: Metastasis is the main cause of cancer-related death governed by both cancer cell-intrinsic properties and extrinsic immune contexture. Our previous reports have suggested critical roles of KIAA1199 in tumor invasion and metastasis in colorectal cancer (CRC). In the present study, we explored the potential effects of KIAA1199 on pre-metastatic niche formation. Methods: The CIBERSORT algorithm analysis for 241 patients with colorectal cancer from the Cancer Genome Atlas was performed to investigate the relationship between KIAA1199 expression and neutrophil accumulation. Neutrophils and T cells were isolated, stimulated and/or cultured for in vitro function assays. Proteins were knocked down in MC38 and HCT116 colorectal cancer cell lines, which were analyzed by immunoblotting and chemotaxis assays. Results: We demonstrate that patients with high KIAA1199 showed an increased level of liver-infıltrating neutrophils, which is further validated using flow cytometry analyses in mouse metastasis model. The increased influx of neutrophils is associated with KIAA1199-driven CRC liver metastasis. Neutrophils isolated from pre-metastatic niche decreased CD8+ T cells infiltration and IFN-r+ CD8+ T cells proportion in vivo. Moreover, they showed a N2-like phenotype and expressed higher level immunosuppressive molecules when exposed to the supernatant of normal CRC cell compared to KIAA1199-knock down cell. In CRC cells, we also found a positive correlation between expression of KIAA1199 and genes that ELR+ chemotaxis of neutrophil (CXCL1/CXCL3/CXCL5), which recruited neutrophils to CRC tumor via CXCR2. Importantly, LY2109761, a TGF-β receptor inhibitor, is sufficient to reduce the mRNA levels of these genes. Furthermore, there is a positive correlation between expression of KIAA1199 and expression of Transforming Growth Factor beta pathway genes (TGFBR1, TGFBR2, and pSMAD3), and further co-immunoprecipitation analysis suggests that KIAA1199 may activate the TGF-β signaling pathway via interacting with the TGFBR1 or TGFBR2. Conclusions: Our data indicate that the upregulation of KIAA1199 may increase the expression of cytokines mediated by TGF-β signaling, which can recruit metastasis-supporting neutrophils to promote colorectal cancer liver metastasis. Blockade of the TGF-β signaling could be a novel therapeutic approach against KIAA1199-high expression CRC.

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Tsujimoto, Hironori, Hiroyuki Horiguchi, Yusuke Matsumoto, Risa Takahata, Nariyoshi Shinomiya, Takao Yamori, Hiromi Miyazaki, et al. "A Potential Mechanism of Tumor Progression during Systemic Infections Via the Hepatocyte Growth Factor (HGF)/c-Met Signaling Pathway." Journal of Clinical Medicine 9, no. 7 (July 1, 2020): 2074. http://dx.doi.org/10.3390/jcm9072074.

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Background: Increasing evidence has demonstrated that postoperative infectious complications (PICs) after digestive surgery are significantly associated with negative long-term outcomes; however, precise mechanisms of how PICs affect the poor long-term survival remain unclear. Here, we focused on the hepatocyte growth factor (HGF)/c-Met signaling pathway as one of those mechanisms. Methods: In the clinical setting, serum HGF levels were measured in the patients with sepsis and those with PICs after undergoing esophagectomy. Using a liver metastasis mouse model with cecal ligation and puncture (CLP), expressions of HGF and the roles of the HGF/c-Met pathway in the progression of tumor cells were examined. Results: Serum HGF levels were very high in the patients with intra-abdominal infection on postoperative days (PODs) 1, 3, and 5; similarly, compared to the patients without PICs, those with PICs had significantly higher serum HGF levels on 1, 3, and 5 days after esophagectomy. The patients with PICs showed poorer overall survival than those without PICs, and the patients with high serum HGF levels on POD 3 showed poorer prognosis than those with low HGF levels. Similarly, at 24 and 72 h after operation, serum levels of HGF in CLP mice were significantly higher than those in sham-operated mice. Intraperitoneal injection of mouse recombinant HGF significantly promoted liver metastases in sham-operated mice on 14 days after surgery. Knocking down c-Met expression on NL17 tumor cells by RNAi technology significantly inhibited the promotion of CLP-induced liver metastases. Conclusions: Infections after surgery increased serum HGF levels in the clinical as well as experimental settings. Induction of high serum HGF levels by CLP promoted liver metastases in a murine liver metastasis model, suggesting the involvement of the HGF/c-Met signaling pathway in tumor promotion mechanisms. Thus, targeting the HGF/c-Met signaling pathway may be a promising approach for malignant tumors, particularly in the patients with PICs.

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Fu, Xiaodan, Bingjing Jiang, Jieting Fu, and Jinli Jia. "MRI Diagnosis and Pathological Examination of Axillary Lymph Node Metastasis in Breast Cancer Patients." Contrast Media & Molecular Imaging 2022 (September 14, 2022): 1–5. http://dx.doi.org/10.1155/2022/4519982.

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In order to explore the characteristics and diagnostic value of magnetic resonance imaging (MRI) in axillary lymph node metastasis of breast cancer, a total of 200 breast cancer patients diagnosed and treated from January 2021 to January 2022 are selected as the study subjects, and 200 patients are divided into an axillary lymph node metastasis group and a simple breast cancer group according to pathological results. The pathological results are used as the gold standard to determine the accuracy and diagnostic efficacy of MRI results. A multivariate logistic regression method is used to analyze the influencing factors of MRI image characteristics of breast cancer axillary lymph node metastasis. The experimental results show that MRI has high application values in diagnosing axillary lymph node metastasis of breast cancer, which is worthy of clinical promotion and application.

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Qin, Z., S. Krüger-Krasagakes, U. Kunzendorf, H. Hock, T. Diamantstein, and T. Blankenstein. "Expression of tumor necrosis factor by different tumor cell lines results either in tumor suppression or augmented metastasis." Journal of Experimental Medicine 178, no. 1 (July 1, 1993): 355–60. http://dx.doi.org/10.1084/jem.178.1.355.

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Tumor necrosis factor (TNF) produced by tumor cells after gene transfer can effectively suppress the growth of locally growing tumors. We wanted to test the effects of "local" TNF on the growth of a highly metastatic cell line. Therefore, a recombinant retrovirus allowing expression of the TNF gene by the beta-actin promotor has been constructed and used to infect the two tumor cell lines EB and ESB, which grow as solid tumor or metastasize, respectively. Expression of TNF by EB cells resulted in their rapid and dose-dependent rejection. In sharp contrast, mice injected with ESB cells producing similar amounts of TNF showed no signs of tumor suppression, but rather had reduced survival rates that correlated with enhanced hepatic metastases. The accelerated formation of liver metastases by ESB TNF cells could be reversed by an anti-TNF mAb. These results demonstrate the opposite effects TNF may have on tumor growth: suppression of a locally growing tumor and promotion of metastasis formation.

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Takahashi, Yuta, Takuya Araki, Ayumu Nagamine, Hideaki Yashima, Daisuke Nagano, Kyoko Obayashi, and Koujirou Yamamoto. "Effect of nicotine- and tar-removed cigarette smoke extract on cancer metastasis." Indonesian Journal of Pharmaceutics 3, no. 2 (November 3, 2021): 49. http://dx.doi.org/10.24198/idjp.v3i2.35909.

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Cigarette smoking is known to impact the promotion of carcinogenesis and tumor metastasis. On the other hand, some components in smoke were found to have health-promoting effects, and cancer suppressor effects of components in tobacco smoke have attracted attention. Although some studies showed the cancer suppressive effect of cigarette smoke extract (CSE) in vitro study, the effect of CSE administration on cancer is controversial. In this study, we investigated the effect of CSE-administration on tumor metastasis in a spontaneous tumor metastasis model using B16-BL6 cells, which is more clinical conditions. C57BL/6NCr mice were subcutaneously inoculated B16-BL6 cells into the footpad of the right rear leg. CSE was intraperitoneally administrated for 28 days from the day of inoculation. At 2 weeks after inoculation, the primary focus was excised. Subsequently, survival days of the mice were recorded to determine the effect of CSE-administration on spontaneous metastasis. The effect of CSE, α, β-unsaturated ketones, and aldehydes on B16-BL6 cell invasiveness were confirmed by matrigel invasion assay. Survival days of mice injected with 100% CSE was significantly shortened than that of control. B16-BL6 cell invasiveness was accelerated by the treatment with 0.1% CSE and 3 μM of crotonaldehyde. Intraperitoneal CSE-administration may progress spontaneous metastasis of B16-BL6 cells via enhancement of B16-BL6 cell invasiveness. As the cause, we found that crotonaldehyde contained in CSE may enhance the invasion ability of cancer cells. To clarify the cancer-suppressing effect of tobacco components, the effect of crotonaldehyde-removed CSE on tumor should be assessed in detail. Keywords: cigarette smoke extract (CSE), metastasis, crotonaldehyde (CA), B16-BL6 mouse melanoma cells, invasion

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Kobayashi, Aya, and Kounosuke Watabe. "Critical role of ADAM15 in tumor progression: targeting multiple factors for metastasis promotion." Future Oncology 4, no. 3 (June 2008): 351–54. http://dx.doi.org/10.2217/14796694.4.3.351.

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Sanz, Guenhaël, Isabelle Leray, Aurélie Dewaele, Julien Sobilo, Stéphanie Lerondel, Stéphan Bouet, Denise Grébert, Régine Monnerie, Edith Pajot-Augy, and Lluis M. Mir. "Promotion of Cancer Cell Invasiveness and Metastasis Emergence Caused by Olfactory Receptor Stimulation." PLoS ONE 9, no. 1 (January 8, 2014): e85110. http://dx.doi.org/10.1371/journal.pone.0085110.

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Liu, Daren, Bogusz Trojanowicz, Longyun Ye, Chao Li, Luqing Zhang, Xiaowen Li, Guogang Li, Yixiong Zheng, and Li Chen. "The Invasion and Metastasis Promotion Role of CD97 Small Isoform in Gastric Carcinoma." PLoS ONE 7, no. 6 (June 29, 2012): e39989. http://dx.doi.org/10.1371/journal.pone.0039989.

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Stefanou, Ekaterini, Angelos Evangelou, and Polycarpos Falaras. "Effects of UV-irradiated titania nanoparticles on cell proliferation, cancer metastasis and promotion." Catalysis Today 151, no. 1-2 (April 2010): 58–63. http://dx.doi.org/10.1016/j.cattod.2010.02.016.

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Shao, L., S. Mori, and T. Kodama. "Positive sentinel lymph nodes biopsy on promotion of cancer metastasis: a negligent effect?" International Journal of Oral and Maxillofacial Surgery 46 (March 2017): 351–52. http://dx.doi.org/10.1016/j.ijom.2017.02.1184.

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Wang, Hui, Xiufei Liu, Min Long, Yi Huang, Linlin Zhang, Rui Zhang, Yi Zheng, et al. "NRF2 activation by antioxidant antidiabetic agents accelerates tumor metastasis." Science Translational Medicine 8, no. 334 (April 13, 2016): 334ra51. http://dx.doi.org/10.1126/scitranslmed.aad6095.

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Cancer is a common comorbidity of diabetic patients; however, little is known about the effects that antidiabetic drugs have on tumors. We discovered that common classes of drugs used in type 2 diabetes mellitus, the hypoglycemic dipeptidyl peptidase–4 inhibitors (DPP-4i) saxagliptin and sitagliptin, as well as the antineuropathic α-lipoic acid (ALA), do not increase tumor incidence but increase the risk of metastasis of existing tumors. Specifically, these drugs induce prolonged activation of the nuclear factor E2–related factor 2 (NRF2)–mediated antioxidant response through inhibition of KEAP1-C151–dependent ubiquitination and subsequent degradation of NRF2, resulting in up-regulated expression of metastasis-associated proteins, increased cancer cell migration, and promotion of metastasis in xenograft mouse models. Accordingly, knockdown ofNRF2attenuated naturally occurring and DPP-4i–induced tumor metastasis, whereas NRF2 activation accelerated metastasis. Furthermore, in human liver cancer tissue samples, increased NRF2 expression correlated with metastasis. Our findings suggest that antioxidants that activate NRF2 signaling may need to be administered with caution in cancer patients, such as diabetic patients with cancer. Moreover, NRF2 may be a potential biomarker and therapeutic target for tumor metastasis.

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Linch, Stefanie N., Melissa J. Kasiewicz, Michael J. McNamara, Ian F. Hilgart-Martiszus, Mohammad Farhad, Peter G. Traber, and William L. Redmond. "Galectin-3 inhibition using novel inhibitor GR-MD-02 improves survival and immune function while reducing tumor vasculature." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 75.9. http://dx.doi.org/10.4049/jimmunol.196.supp.75.9.

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Abstract Immunosuppression and reduced cytotoxic function of tumor-infiltrating lymphocytes (TIL) are major obstacles to creating effective therapies for patients. It is known that Galectin-3 (Gal3), a lectin family member, is expressed and secreted by numerous cancers and immune cell subsets. Serum Gal3 expression is higher in patients with metastatic versus non-metastatic disease, and is associated with reduced survival in metastatic melanoma. Furthermore, Gal3 has been implicated in disease progression via the promotion of angiogenesis and metastasis, the inhibition of TIL function, and promoting M2 polarization of macrophages and mobilization of myeloid cells from the bone marrow to promote a metastatic niche within the tumor. We hypothesized that Gal3 inhibition would improve TIL function while inhibiting the growth and metastasis of tumors. Through collaboration with Galectin Therapeutics, we tested Gal3 inhibition using the novel Gal3 inhibitor, GR-MD-02, with agonist anti-OX40 therapy. We observed that Gal3 inhibition/OX40 agonism improved survival in the MCA-205 sarcoma and 4T-1 mammary carcinoma models, and prolonged survival in the TRAMP-C1 prostate cancer model. Importantly, Gal3 inhibition/OX40 agonism reduced lung metastases in the 4T-1 model. Within the tumor, we observed an increase in the number of proliferating and IFNg-producing TIL. Gal3 inhibition/OX40 agonism was also associated with a decrease in tumor vasculature, as determined by CD31 staining by IHC within the tumors. These studies, along with clinical data from a liver fibrosis trial, supported testing GR-MD-02 in combination with additional immunotherapies to augment T cell function in patients with metastatic melanoma.

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Kasprzak, Aldona, and Agnieszka Adamek. "The Neuropeptide System and Colorectal Cancer Liver Metastases: Mechanisms and Management." International Journal of Molecular Sciences 21, no. 10 (May 15, 2020): 3494. http://dx.doi.org/10.3390/ijms21103494.

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Colorectal cancer (CRC), classified as the third most prevalent cancer worldwide, remains to be a clinical and research challenge. It is estimated that ~50% of CRC patients die from distant metastases, with treatment of this complication still posing significant difficulties. While liver metastasis (LM) cascade is known in the literature, its mechanisms are still unclear and remain studied in different research models. A connection is suggested between nervous system dysfunctions and a range of Neurotransmitters (Nts) (including Neuropeptides, NPs), Neurotrophins (Ntt) and their receptors (Rs) in CRC liver metastasis development. Studies on the role of NP/NP-Rs in the progression and metastasis of CRC, show the complexity of brain–tumor interactions, caused by their different forms of release to the extracellular environment (endocrine, autocrine, paracrine and neurocrine). Many stages of LM are connected to the activity of pro-inflammatory, e.g., Corticotropin-releasing Hormone Receptor 1 (CRHR1), Neuropeptide Y (NPY) and Neurotensin (NT), anti-inflammatory, e.g., Calcitonin Gene-related Peptide (CGRP), CRHR2 and Vasoactive Intestinal Polypeptide (VIP) or dual role neuropeptides, e.g., Substance P (SP). The regulation of the local immunological profile (e.g., CRH/CRHRs), dysfunctions of enteroprotective role of NPs on epithelial cells (e.g., NT/NT-R), as well as structural-functional changes in enteric nervous system innervation of the tumor are also important. More research is needed to understand the exact mechanisms of communication between the neurons and tumor cells. The knowledge on the mechanisms regulating tumor growth and different stages of metastasis, as well as effects of the action of a numerous group of Nts/NPs/Ntt as growth factors, have implications for future therapeutic strategies. To obtain the best treatment outcomes, it is important to use signaling pathways common for many NPs, as well to develop a range of broad-spectrum antagonists. This review aims to summarize the current knowledge on the importance of neuroactive molecules in the promotion of the invasion-metastasis cascade in CRC, as well as the improvements of clinical management of CRC liver metastasis.

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Aprile, G., M. Miscoria, P. Baldin, A. Casetta, M. Pandolfi, C. Di Loreto, S. Pizzolitto, et al. "Chemotherapy-induced thymidine phosphorylase modulation in colorectal cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e15050-e15050. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e15050.

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e15050 Background: Thymidine phosphorylase (TP) is an inducible enzyme responsible for nucleoside metabolism, antiapoptosis activity, and promotion of angiogenesis. In addition, conversion of the prodrug capecitabine (C) to its active form depends on TP activity. Preliminary evidence suggests that TP immunohistochemical expression may predict benefit from first-line treatment of metastatic colorectal cancer (CRC) with C plus irinotecan. Several chemotherapeutic agents have been shown to modulate TP expression. The aim of the present analysis was to verify if TP expression differs among primary and paired metastases in CRC patients, or may vary depending on patients’ exposure to chemotherapy. Methods: TP expression was evaluated by immunohistochemistry (clone p-P-GF.44C, Abcam, Cambridge, UK) in a series of 120 primary CRC and their matched distant metastases. Tsuda's scoring system was adopted, defining TP expression as negative (score 0–1) or positive (score 2–3). Results: Data on the first 57 patients are here presented. Sites of biopsied metastases were liver (n=41), lung (n=10), and peritoneum (n=6). Metastases were asynchronous in 42% of patients. Higher TP expression was observed in primary cancers than in metastases (36.8% vs. 15.8%, p=0.007). Among patients who received at least one cycle of chemotherapy before metastasis sampling (38.6%), a TP expression decrease was demonstrated in only 13% of metastatic samples. Oppositely, a significantly higher proportion of untreated patients lost TP expression in metastasis sites (36%, p=0.01). Conclusions: In advanced CRC patients, TP expression tend to decrease in metastases, particularly in those patients who did not receive chemotherapy before metastatic sampling. Although intratumoral heterogeneity and other causes of discrepancy cannot be excluded, true chemotherapy-induced modulation of TP may be hypothesized. No significant financial relationships to disclose.

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Tzeng, Huey-En, Syuan-Ling Lin, Louis-Anoop Thadevoos, Chih-Yuan Ko, Ju-Fang Liu, Yu-Wen Huang, Chih-Yang Lin, Yi-Chin Fong, and Chih-Hsin Tang. "The mir-423-5p/MMP-2 Axis Regulates the Nerve Growth Factor-Induced Promotion of Chondrosarcoma Metastasis." Cancers 13, no. 13 (July 3, 2021): 3347. http://dx.doi.org/10.3390/cancers13133347.

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A chondrosarcoma is a common tumor of the soft tissue and bone that has a high propensity to metastasize to distant organs. Nerve growth factor (NGF) is capable of promoting the progression and metastasis of several different types of tumors although the effects of NGF in a chondrosarcoma are not confirmed. Here, we found that the levels of NGF and matrix metalloproteinase-2 (MMP-2) correlated with the tumor stage in patients with a chondrosarcoma. NGF facilitated the MMP-2-dependent cellular migration in human chondrosarcoma JJ012 cells while the overexpression of NGF enhanced the lung metastasis in a mouse model of a chondrosarcoma. NGF promoted the MMP-2 synthesis and cell migration by inhibiting miR-423-5p expression through the FAK and c-Src signaling cascades. NGF appears to be a worthwhile therapeutic target in the treatment of a metastatic chondrosarcoma.

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Zhao, Xiulan, Baocun Sun, Yanlei Li, Yanrong Liu, Danfang Zhang, Xudong Wang, Qiang Gu, et al. "Dual effects of collagenase-3 on melanoma: metastasis promotion and disruption of vasculogenic mimicry." Oncotarget 6, no. 11 (February 26, 2015): 8890–99. http://dx.doi.org/10.18632/oncotarget.3189.

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Cook, Leah M., Xuemei Cao, Alexander E. Dowell, Michael T. Debies, Mick D. Edmonds, Benjamin H. Beck, Robert A. Kesterson, et al. "Ubiquitous Brms1 expression is critical for mammary carcinoma metastasis suppression via promotion of apoptosis." Clinical & Experimental Metastasis 29, no. 4 (January 13, 2012): 315–25. http://dx.doi.org/10.1007/s10585-012-9452-x.

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Moller, Andreas. "The role of exosomes in the promotion of epithelial-to-mesenchymal transition and metastasis." Frontiers in Bioscience 25, no. 6 (2020): 1022–57. http://dx.doi.org/10.2741/4846.

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Sundar, Sudha S., and Trivadi S. Ganesan. "Role of Lymphangiogenesis in Cancer." Journal of Clinical Oncology 25, no. 27 (September 20, 2007): 4298–307. http://dx.doi.org/10.1200/jco.2006.07.1092.

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Regional lymph node metastasis is a common event in solid tumors and is considered a marker for dissemination, increased stage, and worse prognosis. Despite rapid advances in tumor biology, the molecular processes that underpin lymphatic invasion and lymph node metastasis remain poorly understood. However, exciting discoveries have been made in the field of lymphangiogenesis in recent years. The identification of vascular endothelial growth factor ligands and cognate receptors involved in lymphangiogenesis, an understanding of the embryology of the mammalian lymphatic system, the recent isolation of pure populations of lymphatic endothelial cells, the investigation of lymphatic metastases in animal models, and the identification of markers that discriminate lymphatics from blood vessels at immunohistochemistry are current advances in the field of lymphangiogenesis, and as such are the main focus of this article. This review also evaluates evidence for lymphangiogenesis (ie, new lymphatic vessel formation in cancer) and critically reviews current data on the prognostic significance of lymphatic vascular density in tumors. A targeted approach to block pathways of lymphangiogenesis seems to be an attractive anticancer treatment strategy. Conversely, promotion of lymphangiogenesis may be a promising approach to the management of treatment-induced lymphedema in cancer survivors. Finally, the implications of these developments in cancer therapeutics and directions for future research are discussed.

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Papadas, Athanasios, Garrett Arauz, Alexander Cicala, Joshua Wiesner, and Fotis Asimakopoulos. "Versican and Versican-matrikines in Cancer Progression, Inflammation, and Immunity." Journal of Histochemistry & Cytochemistry 68, no. 12 (July 6, 2020): 871–85. http://dx.doi.org/10.1369/0022155420937098.

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Versican is an extracellular matrix proteoglycan with key roles in multiple facets of cancer development, ranging from proliferative signaling, evasion of growth-suppressor pathways, regulation of cell death, promotion of neoangiogenesis, and tissue invasion and metastasis. Multiple lines of evidence implicate versican and its bioactive proteolytic fragments (matrikines) in the regulation of cancer inflammation and antitumor immune responses. The understanding of the dynamics of versican deposition/accumulation and its proteolytic turnover holds potential for the development of novel immune biomarkers as well as approaches to reset the immune thermostat of tumors, thus promoting efficacy of modern immunotherapies. This article summarizes work from several laboratories, including ours, on the role of this central matrix proteoglycan in tumor progression as well as tumor-immune cell cross-talk:

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Zhu, Yun, Alfred K. Y. Lam, Daisy K. Y. Shum, Di Cui, Jun Zhang, Dong Dong Yan, Bin Li, et al. "Significance of serglycin and its binding partners in autocrine promotion of metastasis in esophageal cancer." Theranostics 11, no. 6 (2021): 2722–41. http://dx.doi.org/10.7150/thno.49547.

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Journal articles on the topic 'Metastasis promotion'

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