Готові списки джерел за темами / Prostate tumour inducer

Добірка наукової літератури з теми "Prostate tumour inducer"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 29 січня 2023

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Статті в журналах з теми "Prostate tumour inducer"

1

Lanning, Ben, Jason Webber, Pinar Uysal-Onganer, Wen Guo Jiang, Aled Clayton, and Dafydd Alwyn Dart. "Prostate Cancer Cell Extracellular Vesicles Increase Mineralisation of Bone Osteoblast Precursor Cells in an In Vitro Model." Biology 10, no. 4 (April 10, 2021): 318. http://dx.doi.org/10.3390/biology10040318.

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Анотація:
Skeletal metastases are the most common form of secondary tumour associated with prostate cancer (PCa). The aberrant function of bone cells neighbouring these tumours leads to the devel-opment of osteoblastic lesions. Communication between PCa cells and bone cells in bone envi-ronments governs both the formation/development of the associated lesion, and growth of the secondary tumour. Using osteoblasts as a model system, we observed that PCa cells and their conditioned medium could stimulate and increase mineralisation and osteoblasts’ differentiation. Secreted factors within PCa-conditioned medium responsible for osteoblastic changes included small extracellular vesicles (sEVs), which were sufficient to drive osteoblastogenesis. Using MiR-seq, we profiled the miRNA content of PCa sEVs, showing that miR-16-5p was highly ex-pressed. MiR-16 was subsequently higher in EV-treated 7F2 cells and a miR-16 mimic could also stimulate mineralisation. Next, using RNA-seq of extracellular vesicle (EV)-treated 7F2 cells, we observed a large degree of gene downregulation and an increased mineralisation. Ingenuity® Pathway Analysis (IPA®) revealed that miR-16-5p (and other miRs) was a likely upstream effec-tor. MiR-16-5p targets in 7F2 cells, possibly involved in osteoblastogenesis, were included for val-idation, namely AXIN2, PLSCR4, ADRB2 and DLL1. We then confirmed the targeting and dow-regulation of these genes by sEV miR-16-5p using luciferase UTR (untranslated region) reporters. Conversely, the overexpression of PLSCR4, ADRB2 and DLL1 lead to decreased osteoblastogene-sis. These results indicate that miR-16 is an inducer of osteoblastogenesis and is transmitted through prostate cancer-derived sEVs. The mechanism is a likely contributor towards the for-mation of osteoblastic lesions in metastatic PCa.
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2

Pascal, Laura E., Khalid Z. Masoodi, June Liu, Xiaonan Qiu, Qiong Song, Yujuan Wang, Yachen Zang, et al. "Conditional deletion of ELL2 induces murine prostate intraepithelial neoplasia." Journal of Endocrinology 235, no. 2 (November 2017): 123–36. http://dx.doi.org/10.1530/joe-17-0112.

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Анотація:
Elongation factor, RNA polymerase II, 2 (ELL2) is an RNA Pol II elongation factor with functional properties similar to ELL that can interact with the prostate tumor suppressor EAF2. In the prostate, ELL2 is an androgen response gene that is upregulated in benign prostatic hyperplasia (BPH). We recently showed that ELL2 loss could enhance prostate cancer cell proliferation and migration, and that ELL2 gene expression was downregulated in high Gleason score prostate cancer specimens. Here, prostate-specific deletion of ELL2 in a mouse model revealed a potential role for ELL2 as a prostate tumor suppressor in vivo. Ell2-knockout mice exhibited prostatic defects including increased epithelial proliferation, vascularity and PIN lesions similar to the previously determined prostate phenotype in Eaf2-knockout mice. Microarray analysis of prostates from Ell2-knockout and wild-type mice on a C57BL/6J background at age 3 months and qPCR validation at 17 months of age revealed a number of differentially expressed genes associated with proliferation, cellular motility and epithelial and neural differentiation. OncoPrint analysis identified combined downregulation or deletion in prostate adenocarcinoma cases from the Cancer Genome Atlas (TCGA) data portal. These results suggest that ELL2 and its pathway genes likely play an important role in the development and progression of prostate cancer.
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3

Abdulkadir, Sarki A., Jeffrey A. Magee, Thomas J. Peters, Zahid Kaleem, Cathy K. Naughton, Peter A. Humphrey, and Jeffrey Milbrandt. "Conditional Loss of Nkx3.1 in Adult Mice Induces Prostatic Intraepithelial Neoplasia." Molecular and Cellular Biology 22, no. 5 (March 1, 2002): 1495–503. http://dx.doi.org/10.1128/mcb.22.5.1495-1503.2002.

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Анотація:
ABSTRACT The homeodomain-containing transcription factor NKX3.1 is a putative prostate tumor suppressor that is expressed in a largely prostate-specific and androgen-regulated manner. Loss of NKX3.1 protein expression is common in human prostate carcinomas and prostatic intraepithelial neoplasia (PIN) lesions and correlates with tumor progression. Disruption of the murine Nkx3.1 gene results in defects in prostate branching morphogenesis, secretions, and growth. To more closely mimic the pattern of NKX3.1 loss that occurs in human prostate tumors, we have used Cre- and loxP-mediated recombination to delete the Nkx3.1 gene in the prostates of adult transgenic mice. Conditional deletion of one or both alleles of Nkx3.1 leads to the development of preinvasive lesions that resemble PIN. The pattern of expression of several biomarkers (Ki-67, E-cadherin, and high-molecular-weight cytokeratins) in these PIN lesions resembled that observed in human cases of PIN. Furthermore, PIN foci in mice with conditional deletion of a single Nkx3.1 allele lose expression of the wild-type allele. Our results support the role of NKX3.1 as a prostate tumor suppressor and indicate a role for this gene in tumor initiation.
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4

Bronte, Vincenzo, Tihana Kasic, Giorgia Gri, Keti Gallana, Giovanna Borsellino, Ilaria Marigo, Luca Battistini, et al. "Boosting antitumor responses of T lymphocytes infiltrating human prostate cancers." Journal of Experimental Medicine 201, no. 8 (April 11, 2005): 1257–68. http://dx.doi.org/10.1084/jem.20042028.

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Анотація:
Immunotherapy may provide valid alternative therapy for patients with hormone-refractory metastatic prostate cancer. However, if the tumor environment exerts a suppressive action on antigen-specific tumor-infiltrating lymphocytes (TIL), immunotherapy will achieve little, if any, success. In this study, we analyzed the modulation of TIL responses by the tumor environment using collagen gel matrix–supported organ cultures of human prostate carcinomas. Our results indicate that human prostatic adenocarcinomas are infiltrated by terminally differentiated cytotoxic T lymphocytes that are, however, in an unresponsive status. We demonstrate the presence of high levels of nitrotyrosines in prostatic TIL, suggesting a local production of peroxynitrites. By inhibiting the activity of arginase and nitric oxide synthase, key enzymes of L-arginine metabolism that are highly expressed in malignant but not in normal prostates, reduced tyrosine nitration and restoration of TIL responsiveness to tumor were achieved. The metabolic control exerted by the tumor on TIL function was confirmed in a transgenic mouse prostate model, which exhibits similarities with human prostate cancer. These results identify a novel and dominant mechanism by which cancers induce immunosuppression in situ and suggest novel strategies for tumor immunotherapy.
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5

Song, Liankun, Vyvyan Nguyen, Shan Xu, Jana Yamak, Kia Arabzadehkaffash, Ali Fazelpour, Merci Mino, Matthew Tippin, Shuang Meng, and Xiaolin Zi. "Abstract 1: Transcriptional profiling of prostatic Skp2 knock-in mouse model and development of the associated prostate organoids for testing Skp2 targeting agents." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1. http://dx.doi.org/10.1158/1538-7445.am2022-1.

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Анотація:
Abstract S-phase kinase associated protein 2 (Skp2) is a promising drug target as studies have demonstrated that Skp2 is required for spontaneous tumor development that occurs in the retinoblastoma protein (pRb), Pten, or p53 deficient mice. We, therefore, aim to establish CRISPR human Skp2 (hSkp2) knock-in in the prostates of mice to study the molecular profiling features in prostate carcinogenesis. Prostate weights increased in transgenic mice and overexpression of hSkp2 induced prostatic lesions including hyperplasia, mouse prostate intraepithelial neoplasia (mPIN), and carcinoma, which suggested the initial role of hSkp2 in early prostate carcinogenesis. RNAseq results revealed Myl3 and Ctgf as the top down-expressed and up-expressed genes respectively in hSkp2 mice prostates. Gene set enrichment analysis (GSEA) demonstrated the significant upregulations of ribosome and proteasome pathways which had similar alterations in the human prostate cancer dataset with Skp2 overexpression, suggesting the potential role of ribosome biogenesis in prostate tumorigenesis and for drug development. In addition, Skp2 organoids derived from transgenic mice prostates were being developed for convenient and efficient screening of specific Skp2 inhibitors. Flavokawain A (FKA) and Skp2 inhibitor C1 both selectively decreased the viability and altered the morphologies of hSkp2 organoids, meanwhile FKA exhibited less toxicity on wild-type organoids. Citation Format: Liankun Song, Vyvyan Nguyen, Shan Xu, Jana Yamak, Kia Arabzadehkaffash, Ali Fazelpour, Merci Mino, Matthew Tippin, Shuang Meng, Xiaolin Zi. Transcriptional profiling of prostatic Skp2 knock-in mouse model and development of the associated prostate organoids for testing Skp2 targeting agents [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1.
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6

Ketteler, Julia, Andrej Panic, Henning Reis, Alina Wittka, Patrick Maier, Carsten Herskind, Ernesto Yagüe, Verena Jendrossek, and Diana Klein. "Progression-Related Loss of Stromal Caveolin 1 Levels Mediates Radiation Resistance in Prostate Carcinoma via the Apoptosis Inhibitor TRIAP1." Journal of Clinical Medicine 8, no. 3 (March 12, 2019): 348. http://dx.doi.org/10.3390/jcm8030348.

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Анотація:
Tumour resistance to chemo- and radiotherapy, as well as molecularly targeted therapies, limits the effectiveness of current cancer treatments. We previously reported that the radiation response of human prostate tumours is critically regulated by CAV1 expression in stromal fibroblasts and that loss of stromal CAV1 expression in advanced tumour stages may contribute to tumour radiotherapy resistance. Here we investigated whether fibroblast secreted anti-apoptotic proteins could induce radiation resistance of prostate cancer cells in a CAV1-dependent manner and identified TRIAP1 (TP53 Regulated Inhibitor of Apoptosis 1) as a resistance-promoting CAV1-dependent factor. TRIAP1 expression and secretion was significantly higher in CAV1-deficient fibroblasts and secreted TRIAP1 was able to induce radiation resistance of PC3 and LNCaP prostate cancer cells in vitro, as well as of PC3 prostate xenografts derived from co-implantation of PC3 cells with TRIAP1-expressing fibroblasts in vivo. Immunohistochemical analyses of irradiated PC3 xenograft tumours, as well as of human prostate tissue specimen, confirmed that the characteristic alterations in stromal-epithelial CAV1 expression were accompanied by increased TRIAP1 levels after radiation in xenograft tumours and within advanced prostate cancer tissues, potentially mediating resistance to radiation treatment. In conclusion, we have determined the role of CAV1 alterations potentially induced by the CAV1-deficient, and more reactive, stroma in radio sensitivity of prostate carcinoma at a molecular level. We suggest that blocking TRIAP1 activity and thus avoiding drug resistance may offer a promising drug development strategy for inhibiting resistance-promoting CAV1-dependent signals.
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7

Layman, Awo Akosua K., Shivam Joshi, and Sanjeev Shah. "Metastatic prostate cancer presenting as tumour-induced osteomalacia." BMJ Case Reports 12, no. 7 (July 2019): e229434. http://dx.doi.org/10.1136/bcr-2019-229434.

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Анотація:
Tumour-induced osteomalacia (TIO), or oncogenic osteomalacia, is a paraneoplastic syndrome marked by hypophosphataemia, renal phosphate wasting, bone pain, weakness, and fractures. The syndrome has been reported with both benign and malignant tumours including parotid gland basal cell tumours, thyroid carcinomas, colon adenocarcinomas, and prostate cancer. Often, the syndrome is marked by an insidious course during which patients present with generalised bony pain and weakness, which do not resolve until the underlying tumour is identified and treated. We present a case of a patient with Parkinson’s disease whose subacute weakness, lower extremity paresis, and renal phosphate wasting led to the synchronous diagnosis of metastatic prostate adenocarcinoma and TIO.
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8

Ene, Cosmin-Victor, Ilinca Nicolae, Bogdan Geavlete, Petrisor Geavlete, and Corina Daniela Ene. "IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis." Analytical Cellular Pathology 2022 (April 12, 2022): 1–10. http://dx.doi.org/10.1155/2022/5980387.

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Анотація:
Benign prostatic hyperplasia and prostate cancer are tumoral pathologies characterized by the overexpression of inflammatory processes. The exploration of tumor microenvironment and understanding the sequential events that take place in the stromal area of the prostate could help for an early management of these pathologies. This way, it is feasible the hypothesis that normalizing the stromal environment would help to suppress or even to reverse tumor fenotype. A number of immunological and genetic factors, endocrine dysfunctions, metabolic disorders, infectious foci, nutritional deficiencies, and chemical irritants could be involved in prostate tumor development by maintaining inflammation, affecting local microcirculation, and promoting oxidative stress. Inflammatory processes activate hyperproliferative programs that ensure fibromuscular growth of the prostate and a number of extracellular changes. Acute and chronic inflammations cause accumulation of immunocompetent cells in affected prostate tissue (T cells, macrophages, mastocytes, dendritic cells, neutrophils, eosinophils, monocytes). Prostate epithelial and stromal cells, peri-prostatic fat cells, prostatic microvascular endothelial cells, and inflammatory cells produce cytokines, generating a local inflammatory environment. Interleukin-6 (IL-6) proved to be involved in the prostate tumor pathogenesis. IL-6 ability to induce pro- and anti-inflammatory responses by three mechanisms of signal transduction (classical signaling, transsignaling, cluster signaling), to interact with a diversity of target cells, to induce endocrine effects in an autocrine/paracrine manner, and the identification of an IL-6 endogenous antagonist that blocks the transmission of IL-6 mediated intracellular signals could justify current theories on the protective effects of this cytokine or by alleviating inflammatory reactions or by exacerbating tissue damage. This analysis presents recent data about the role of the inflammatory process as a determining factor in the development of benign and malign prostate tumors. The presented findings could bring improvements in the field of physiopathology, diagnosis, and treatment in patients with prostate tumors. Modulation of the expression and activity of interleukin-6 could be a mean of preventing or improving these pathologies.
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9

Sass, Stephanie N., and Sandra O. Gollnick. "Tumor-associated myeloid cells convert indolent prostate cancer to aggressive disease." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 73.21. http://dx.doi.org/10.4049/jimmunol.196.supp.73.21.

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Анотація:
Abstract Difficulties differentiating indolent from progressing prostate cancer (CaP) results in ineffective treatment strategies. Tumor-associated myeloid cells (TAMC) contribute to tumor progression; yet the role TAMC play in the conversion from indolent to progressing CaP is unclear. To test whether TAMC promote CaP progression we developed a murine model using two isogenic cell lines from the TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model. Tumorigenic C2 cells mimic progressing disease while non-tumorigenic C3 cells represent indolent disease. We report for the first time that CD11b+ TAMC isolated from C2 tumors co-injected with the non-tumorigenic C3 cells drive C3 tumor growth. In contrast, TAMC isolated from C2 tumor-bearing spleens or naïve spleens did not promote C3 tumor growth. This is the first indication that TAMC drive progression of indolent disease. Strikingly, tumor cells explanted from TAMC-induced C3 tumors were tumorigenic in the absence of additional TAMC, suggesting that TAMC induce stable changes within the C3 cells. These results have been recapitulated with the non-tumorigenic human cell line BPH-1 (benign prostatic hyperplasia). Furthermore, TAMC-induced tumor growth occurs via a TAMC secreted factor. Using a 5-day transwell system PC3M (human prostatic adenocarcinoma) TAMC were able to drive BPH-1 tumorigenesis. Future work will determine the factor secreted by TAMC and identify the molecular mechanisms responsible for tumor promotion. This work has the potential to identify critical factors responsible for the conversion of indolent to progressing disease thus laying the groundwork for novel prognostic and therapeutic strategies.
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10

Boutillon, Pigat, Sala, Reyes-Gomez, Moriggl, Guidotti, and Goffin. "STAT5a/b Deficiency Delays, but does not Prevent, Prolactin-Driven Prostate Tumorigenesis in Mice." Cancers 11, no. 7 (July 2, 2019): 929. http://dx.doi.org/10.3390/cancers11070929.

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Анотація:
The canonical prolactin (PRL) Signal Transducer and Activator of Transcription (STAT) 5 pathway has been suggested to contribute to human prostate tumorigenesis via an autocrine/paracrine mechanism. The probasin (Pb)-PRL transgenic mouse models this mechanism by overexpressing PRL specifically in the prostate epithelium leading to strong STAT5 activation in luminal cells. These mice exhibit hypertrophic prostates harboring various pre-neoplastic lesions that aggravate with age and accumulation of castration-resistant stem/progenitor cells. As STAT5 signaling is largely predominant over other classical PRL-triggered pathways in Pb-PRL prostates, we reasoned that Pb-Cre recombinase-driven genetic deletion of a floxed Stat5a/b locus should prevent prostate tumorigenesis in so-called Pb-PRLSTAT5 mice. Anterior and dorsal prostate lobes displayed the highest Stat5a/b deletion efficiency with no overt compensatory activation of other PRLR signaling cascade at 6 months of age; hence the development of tumor hallmarks was markedly reduced. Stat5a/b deletion also reversed the accumulation of stem/progenitor cells, indicating that STAT5 signaling regulates prostate epithelial cell hierarchy. Interestingly, ERK1/2 and AKT, but not STAT3 and androgen signaling, emerged as escape mechanisms leading to delayed tumor development in aged Pb-PRLSTAT5 mice. Unexpectedly, we found that Pb-PRL prostates spontaneously exhibited age-dependent decline of STAT5 signaling, also to the benefit of AKT and ERK1/2 signaling. As a consequence, both Pb-PRL and Pb-PRLSTAT5 mice ultimately displayed similar pathological prostate phenotypes at 18 months of age. This preclinical study provides insight on STAT5-dependent mechanisms of PRL-induced prostate tumorigenesis and alternative pathways bypassing STAT5 signaling down-regulation upon prostate neoplasia progression.
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Більше джерел

Дисертації з теми "Prostate tumour inducer"

1

Markowski, Mark Christopher. "Inflammatory cytokines induce ubiquitination and loss of the prostate suppressor protein NKX3.1." Connect to Electronic Thesis (CONTENTdm), 2008. http://worldcat.org/oclc/454182234/viewonline.

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2

Anzenberg, Vered. "LET dependence of radiation-induced bystander effects using human prostate tumor cells." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/44795.

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Анотація:
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Nuclear Science and Engineering, 2008.
"June 2008."
Includes bibliographical references (leaves 133-140).
In the past fifteen years, evidence provided by many independent research groups have indicated higher numbers of cells exhibiting damage than expected based on the number of cells traversed by the radiation. This phenomenon has been coined as the "bystander effect". The purpose of this study was to characterize the ability of irradiated tumor cells to induce bystander effects in co-cultured cells. Human DU-145 prostate carcinoma cells were grown on a 1.4 [mu]m-thick mylar membrane in specially constructed cell culture dishes for irradiation with alpha particles (average energy 3.14 MeV) from a 241Am source, or in 6-well plates for irradiation with 250 kVp x-rays at 25°C. In parallel experiments, the tumor cells were incubated at 4°C for one hour prior to irradiation and irradiated on ice to test the nature of the bystander signal. Bystander cells were placed into the medium above the irradiated DU-145 and were co-incubated for a length of time. The bystander effect endpoints measured in either DU-145 tumor cells or in normal primary AGO1522 fibroblasts were micronucleus (MN) formation, [gamma]-H2AX double strand break repair foci, and survival fraction. A 1.5-2.0-fold increase in MN formation was observed in both DU-145 and AG01522 bystander cells after either alpha particle or xray irradiation of the DU-145 target cells. A 1.5-fold [gamma]-H2AX bystander increase and a survival fraction reduction to 80% were only detected in AGO1522 cells, and only after xray irradiation of target DU-145 cells. Alpha particle irradiation of the target DU-145 cells produced neither [gamma]-H2AX foci nor survival fraction bystander effect in either cell line. Lowering the temperature to 4°C during the irradiation of the DU-145 tumor cells, with either x-rays or alpha particles, eliminated both the MN formation and the decreased survival fraction bystander effects in the co-cultured AG01522 fibroblasts.
(cont.) This study demonstrates that biochemical processes in the directly-irradiated tumor cells are required for initiation of the signaling process. Low temperature during the irradiation inhibited the initiation of a bystander signal. There are also LET-dependent differences in the signal released from DU-145 human prostate carcinoma cells; and that, for some endpoints, bystander AG01522 fibroblasts and bystander DU-145 prostate carcinoma cells respond differently to the same, medium-mediated signal.
by Vered Anzenberg.
Ph.D.
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3

Leclercq, Tamara Marie. "Regulation of sphingosine kinase by interacting proteins." Thesis, 2010. http://hdl.handle.net/2440/64752.

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Анотація:
Sphingosine kinase 1 (SK1) is responsible for phosphorylating the lipid sphingosine, generating the bio-active phospholipid, sphingosine 1-phosphate (S1P). Cells possess basal SK1 activity which has been proposed to serve in a ‘housekeeping’ function to limit the levels of proapoptotic sphingosine and ceramide in the cell. In some circumstances, however, such as cell exposure to growth factors and cytokines this basal level of SK1 activity is increased, resulting in an increased production of S1P. As S1P is a pro-proliferative, pro-survival molecule, its increased production is associated with enhanced cell proliferation, survival and an oncogenic phenotype. The Pitson laboratory has shown previously that one mechanism by which SK1 is activated is through phosphorylation at Ser-225 by ERK1/2. Here, my studies focused on alternative mechanisms of SK1 activation that arise through its interaction with two proteins, eukaryotic elongation factor 1A (eEF1A) and a relatively uncharacterised protein, SK activator molecule 1 (SKAM). eEF1A is able to directly increase the catalytic activity of SK1 in vitro and is also able to increase endogenous SK activity when over-expressed in quiescent cells that have reduced levels of endogenous eEF1A protein. Due to the abundance of eEF1A protein within a cell, I hypothesized that the effect of eEF1A on SK activity may be dynamically regulated. eEF1A contains a ‘G protein-like’ domain that enables it to bind GDP and GTP. When bound by GTP, eEF1A undergoes a large conformational change that enables it to bind aminoacyltRNA for transport to the ribosome. Similarly, just as the nucleotide-bound state of eEF1A regulates its role in protein synthesis, I found that the nucleotide-bound state of eEF1A also regulates its ability to activate SK1. Strikingly, it is only the translationally inactive eEF1A.GDP that can activate SK1. A truncated form of eEF1A named PTI-1 has been described that lacks the ‘G protein-like’ domain and thus can not bind guanine nucleotides, rendering it structurally analogous to eEF1A.GDP. In keeping with my finding that only eEF1A.GDP activates SK1, I found that PTI-1 also activates SK1 both in vitro and in cells. Importantly, PTI-1 has been previously characterized as an oncoprotein and for the first time my studies have shown a likely mechanism by which PTI-1 induces a tumourigenic phenotype. Expression of PTI-1 in NIH 3T3 cells induces neoplastic transformation, as measured by focus formation. Notably, this PTI-1-induced transformation is blocked when cells are treated with SK inhibitors or when cells are co-transfected with PTI-1 and a dominant negative SK1, indicating that oncogenesis by PTI-1 is mediated through SK1. The current study also investigated the regulation of SK1 activity by its interaction with SKAM1. Previous studies have shown that SKAM1, like eEF1A, can directly increase the catalytic activity of SK1 in vitro and in cells. My studies have determined the minimal region of interaction of SKAM1 that is still able to interact with and activate SK1. Remarkably, a 35 amino acid SKAM1 peptide retained the ability to activate SK1. The physiological relevance of the SK1-SKAM1 interaction was also examined and I have shown that knock-down of SKAM1, and the related protein SKAM2, in HEK 293T cells resulted in decreased cell proliferation coupled with increased susceptibility to apoptosis. Results presented here, also suggest that phosphorylation of SKAM1 at Tyr-46 acts as a negative regulator for SKAM1-induced SK1 activation. In summary, the current study presents two novel SK1 interacting proteins that directly increase the catalytic activity of this enzyme, and investigates mechanisms by which their effects on SK1 activity are regulated. While the guanine nucleotide bound state of eEF1A1 determines its effects on SK1 activity, the phosphorylation status of SKAM1 appears to determine its ability to activate SK1.
Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2010
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4

Walker, Tristan J. "The association of infiltrating lymphocytes in androgen ablation induced apoptosis of prostate tumours." Thesis, 2005. http://hdl.handle.net/2429/16799.

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Анотація:
Prostate cancer has a high incidence and mortality rate, with currently no curative treatment for advanced disease. Both the gland and the tumour are androgen dependent; therefore, the removal of androgens, known clinically as hormone ablation therapy, is the most effective treatment, and is thought to force secretory epithelial cells, as well as the cancerous tissue, to undergo apoptosis. Unfortunately, the effects of the hormone ablative therapy are temporary and prostate cancer will recur in an untreatable androgen independent phenotype. The underlying molecular mechanisms involved in prostate cancer progression and the effects of androgen ablation are poorly understood, and the process by which the cancer is cleared, post-androgen ablation, has never been clearly elucidated. This study proposes that, contrary to present theorem, androgen ablation itself is insufficient to induce apoptosis; rather, the apoptotic reaction is facilitated by immune factors including the presence of immune cells at the tumour site. Observational data was used in conjunction with microarray experiments and immunohistochemistry to identify underlying gene expression and immune cell components of tumours grown in hosts with varying states of immunocompentency. We demonstrate that the immunocompetency of the host affects the rate of tumour regression post androgen ablation. Our results show that a tumour in a host with a functional immune system will regress faster and reach its nadir point sooner than in B- or T-cell deficient animals. Furthermore, lymphocyte infiltration significantly changes at the point at which the tumour reaches its lowest point. This correlates with gene expression studies showing a shift towards up-regulating genes related to antigen presentation and immune function. Immunohistochemistry on human tissue samples analyzed from radical prostatectomies also show a marked increase in lymphocyte infiltration post androgen ablation. A better understanding of the tumour environment and effecter immune factors present will provide additional clinical strategies and therapeutic targets to better facilitate androgen ablation therapy.
Medicine, Faculty of
Medical Genetics, Department of
Graduate
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5

Hsiao, Fu-Ching, and 蕭富擎. "Hispolon Inhibits Angiogenesis By Suppressing Vascular Endothelial Growth Factor Signaling Pathway And induces Prostate Tumor Cell apoptosis." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/82330016299966227600.

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Анотація:
碩士
中國醫藥大學
中國藥學研究所碩士班
97
Phellinus linteus (PL) , is a traditional medicinal plant of oriental people (especially in China, Japan,and North Korea ) , was demonstrated to exhibit anti-bacterial , anti-tumour , anti-fibrotic , anti-oxidant and anti-inflammation functions in several studies. Hispolon is a major component of PL with great antioxidant activity. Whether Hispolon induces prostate tumor cell apoptosis or inhibits angiogenesis,which is crucial for cancer and other human diseases, remains unknown. First, we investigated how hispolon induce apoptosis in the prostate tumor cell lines PC-3. In the MTT assay, treatment of Hispolon inhibited the growth of PC-3 in the dose- and time- dependent manners. Next ,Hispolon inducing PC-3 cells apoptosis was confirmed by nuclear condensation (DAPI staining), DNA fragmentation assay and Annexin V-FITC/PI staining . We also examined the Hispolon induced cell cycle arrest in the G2 phase by flow cytometric analysis. In vitro angiogenesis study, we found that Hispolon effectively inhibited human umbilical vein endothelial cell migration, invasion, and tube formation. In a coculture study, Hispolon completely prevented U87MG cell–mediated capillary formation of HUVEC. This inhibitor also prevented that VEGF and MMP induced migration ability of HUVEC when cultured alone or cocultured with U87MG cells. In vivo angiogenesis study, we use the rat aortic ring assay, chicken chorioallantoic membrane assay (CAM) and Matrigel plug assay to evaluate anti-angiogenic effects. Finally, Western blot showed that Hispolon treatment suppressed the protein expression of TIMP-1 , PAI-1 , PI3K , AKT , P44/42 , phospho-P44/42 , RAS , NF-κB and COX-2, which were involved in endothelial cell survival, proliferation, migration and angiogeneis. Our results indicated that Hispolon exerted an anti-tumor activity associated with decreased proliferation of tumor cells and induced the apoptosis of prostate tumor cell, and inhibited the anti-angiogenic activity by VEGF signaling pathway .
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Частини книг з теми "Prostate tumour inducer"

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Sarkar, Dipak K. "Fetal Alcohol Exposure Increases Susceptibility to Carcinogenesis and Promotes Tumor Progression in Prostate Gland." In Biological Basis of Alcohol-Induced Cancer, 389–402. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09614-8_23.

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Hermanus Johannes Sliepen, Sonny. "Bone Cancer Pain, Mechanism and Treatment." In Recent Advances in Bone Tumours and Osteoarthritis. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95910.

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The world health organization (WHO) has predicted a global amount of 19 million cancer cases by 2025. Breast, prostate and lung cancer are common cancer types and show metastasis in 60 to 84% of the cases, with 75 to 90% experiencing life-altering cancer-induced bone pain (CIBP), characterized by continuous, dull progressive pain with movement-induced incident peaks and random breakthrough spikes. Therefore, it is the most difficult pain condition to treat. CIBP is a unique type of pain with neuropathic and nociceptive components. Briefly, an invading tumor cell disturbs the healthy balance of the bone resulting in an acidic microenvironment, activating sensory fibers in the bone. The invaded tumor cell and adjacent stromal cells secrete mediators initiating an immune response with transcriptional signaling, resulting in increased cytokines and growth factors. Sensory nerve fibers are damaged and start to sprout, causing ectopic firing, and as tumors grow in size they activate mechanoreceptors. Aside from bisphosphonates and antibody therapy, CIBP is treated by a range of NSAIDs to strong opioids, but remains undertreated in one-third of cases. This chapter discusses the accompanying CIBP of bone tumors, the mechanism of action and current treatments.
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Morello, Matteo, Gustavo E. Ayala, Fabiana Rosati, Giovanna Danza, Rile Li, Anna Frolov, Rosalyn M. Adam, et al. "Loss of Caveolin-1 Increases Tumor Cell Migration, Is Predictive of Disease-Free Survival, and Induces Steroidogenesis in Prostate-Derived Fibroblasts." In TRANSLATIONAL - Steroidal Regulation of Breast & Prostate Cancer, OR06–6—OR06–6. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.or7.or06-6.

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Тези доповідей конференцій з теми "Prostate tumour inducer"

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Attaluri, Anilchandra, Ronghui Ma, and Liang Zhu. "Temperature Elevations in Implanted Prostatic Tumors in Mice During Magnetic Nanoparticle Hyperthermia: In Vivo Experimental Study." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53128.

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In this study, we perform in vivo animal experiments on implanted prostatic tumors in mice to measure temperature elevation distribution in the tumor during magnetic nanoparticle hyperthermia. Temperature rises are induced by a commercially available ferrofluid injected to the center of the tumor, which is subject to an alternating magnetic field. Temperature mapping in the implanted prostatic tumors during the heating has illustrated the feasibility of elevating the tumor temperature higher than 50°C using only 0.1 cc ferrofluid injected in the tumor and under a relatively low magnetic field (3 kA/m). Ferrofluid infusion rates during intratumoral injection may affect nanoparticle spreading in tumors. Using a very slow infusion rate of 5 μ1/min results in an average temperature elevation in tumors 27°C above the baseline temperatures of 37°C. However, the temperature elevations are barely 14°C when the infusion rate is 20 μl/min. Our results suggest a more confined nanoparticle distribution to the injection site using smaller infusion rates.
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Manuchehrabadi, N., A. Attaluri, H. Cai, R. Edziah, E. Lalanne, C. Bieberich, R. Ma, A. M. Johnson, and L. Zhu. "Visualization and Quantification of Gold Nanorods Distribution in Prostatic Tumors Using MicroCT Imaging." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80317.

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One uncertainty in use of gold nanorods for laser photothermal therapy is the non-uniform spreading of gold nanorods in tissue after either systemic delivery or intratumoral injections. High concentration of gold nanorods in certain areas influences the resulted optical absorption of the laser and thermal damage to tumors. This also provides challenges in designing optimal heating protocols via modeling thermal transport in laser photothermal therapy. For successful cancer treatment, the tissue should be heated with minimum thermal dosage to induce tumor cell damage, while minimizing overheating in the surrounding healthy tissues. Thus, one of the main challenges for reliable cancer therapy is to precisely control loading and distribution of gold nanorods in the tumour tissue. The critical mass transport processes are the distribution of gold nanorods after injection to the tumor and the redistribution of gold nanorods during laser treatment. Since tumors are opaque, nanostructure distribution in tissue is often studied either by theoretical modeling approaches1, or via dye enhanced imaging on superficial layers of tumors.2 It is important to find a technique which can directly visualize and analyze three-dimensional nanostructure distribution of tumors. Three-dimensional reconstructions of tumors with the ability to trace gold nanorod spreading have the potential for precise theoretical simulation of temperature fields. Previous studies showed that computer tomography (CT) scan is a promising technique to be utilized to characterize the distribution of intratumorally injected magnetic nanoparticles in tumors 3.
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Crawford, Alison, Kristin Vazzana, Jeffrey VanValkenburgh, Lauric Haber, Jennifer Principio, Cagan Gurer, Kara Olson, Eric Smith, Gavin Thurston, and Jessica R. Kirshner. "Abstract A193: Fully human bispecific antibodies induce potent anti-tumor effects against prostate tumors in mice." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-a193.

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Ko, Chun-Jung, Ying-Chieh Lu, Pee-Fang Lai, Pei-Wen Hsiao, and Ming-Shyue Lee. "Abstract B67: Matriptase is involved in COX-2 signaling-induced prostate cancer cell invasion." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-b67.

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Fang, Lei-Ya, Kouji Izumi, and Wen-Jye Lin. "Abstract C229: Tumor-associated macrophages induce prostate tumorigenesis via CCL4/STAT3 signals." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c229.

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Pan, Chunliu, Yanni Zulia, and Kent L. Nasituk. "Abstract B092: Myokine signaling blockade prevents androgen deprivation therapy-induced sarcopenia and promotes prostate tumor regression." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-b092.

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Sharma, Sambad, Fei Xing, Yin Liu, Kerui Wu, Aya Kobayashi, and Kounosuke Watabe. "Abstract 3206: SPARC in tumor microenvironment induces dormancy of prostate cancer in bone." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3206.

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Coleman, C. Norman, Molykutty John-Aryankalayil, Adeola Y. Makinde, and Sanjeewani T. Palayoor. "Abstract 425: Fractionated radiation-induced tumor suppressor microRNAs in human prostate carcinoma cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-425.

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El-Kenawi, Asmaa, William Dominguez Viqueira, Min Liu, Shivanshu Awasthi, Jasreman Dhillon, Kosj Yamoah, Xiaoqing Yu, John Koomen, Robert Gatenby, and Brian Ruffell. "Abstract 734: Macrophage tumor cell metabolic interactions induce therapeutic resistance in prostate cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-734.

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Cordonnier, Thomas, Jennifer L. Bishop, Masaki Shiota, Ario Takeuchi, Ka Mun Nip, Martin Gleave, and Amina Zoubeidi. "Abstract C25: Hsp27 is required for EGF-induced epithelial to mesenchymal transition in prostate cancer." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-c25.

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Звіти організацій з теми "Prostate tumour inducer"

1

Chai, Karl X. Signal Transduction Pathway in Maspin-Induced Tumor Suppression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada395750.

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Bushman, Wade, and Aubie Shaw. Identification of Sonic Hedgehog-Induced Stromal Factors That Stimulate Prostate Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada484566.

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Yang, Feng. Novel Therapeutic Targets to Inhibit Tumor Microenvironment-Induced Castration-Resistant Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613723.

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Shaw, Aubie, and Wade Bushman. Identification of Sonic Hedgehog-Induced Stromal Factors That Stimulate Prostate Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada466565.

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Xing, Fei. BMP7 Induces Dormancy of Prostatic Tumor Stem Cell in Bone. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada570860.

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Xing, Fei. BMP7 Induces Dormancy of Prostatic Tumor Stem Cell in Bone. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada592100.

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Kobayashi, Aya. BMP7 Induces Dormancy of Prostatic Tumor Stem Cell in Bone. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada553888.

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