Academic literature on the topic 'Cancer, differentiation, NMR, colon cell lines'

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Journal articles on the topic "Cancer, differentiation, NMR, colon cell lines"

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Park, Hyun, Nguyen Tuan, Joonseok Oh, Younglim Son, Mark Hamann, Robert Stone, Michelle Kelly, Sangtaek Oh, and MinKyun Na. "Sesterterpenoid and Steroid Metabolites from a Deep-Water Alaska Sponge Inhibit Wnt/β-Catenin Signaling in Colon Cancer Cells." Marine Drugs 16, no. 9 (August 27, 2018): 297. http://dx.doi.org/10.3390/md16090297.

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The Wnt/β-catenin signaling pathway is known to play critical roles in a wide range of cellular processes: cell proliferation, differentiation, migration and embryonic development. Importantly, dysregulation of this pathway is tightly associated with pathogenesis in most human cancers. Therefore, the Wnt/β-catenin pathway has emerged as a promising target in anticancer drug screening programs. In the present study, we have isolated three previously unreported metabolites from an undescribed sponge, a species of Monanchora (Order Poecilosclerida, Family Crambidae), closely related to the northeastern Pacific species Monanchora pulchra, collected from deep waters off the Aleutian Islands of Alaska. Through an assortment of NMR, MS, ECD, computational chemical shifts calculation, and DP4, chemical structures of these metabolites have been characterized as spirocyclic ring-containing sesterterpenoid (1) and cholestane-type steroidal analogues (2 and 3). These compounds exhibited the inhibition of β-catenin response transcription (CRT) through the promotion of β-catenin degradation, which was in part implicated in the antiproliferative activity against two CRT-positive colon cancer cell lines.
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Matusiak, Damien, Sarah Glover, Rajkumar Nathaniel, Kristina Matkowskyj, Jianxin Yang, and Richard V. Benya. "Neuromedin B and its receptor are mitogens in both normal and malignant epithelial cells lining the colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 4 (April 2005): G718—G728. http://dx.doi.org/10.1152/ajpgi.00156.2004.

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Bombesin-like peptides are uniformly thought to act as mitogens in cancer. Yet by studying human tissues, we have recently shown that bombesin and its mammalian homologue gastrin-releasing peptide act as morphogens, promoting tumor differentiation when aberrantly upregulated in colon cancer. In contrast, little is known about the bombesin-like peptide neuromedin B (NMB) and its receptor (NMB-R) in the human gastrointestinal tract. We therefore studied their presence and function in normal and malignant human colonic epithelia. Anti-NMB monoclonal antibodies were made against keyhole limpet hemocyanin (KLH)-conjugated human NMB, whereas anti-NMB-R antibodies were raised in rabbits against KLH-conjugated peptides corresponding to the third intracellular loop and COOH-terminal tail of the receptor protein. NMB antibody recognized two bands at ∼1.2 kDa and ∼1.5 kDa. NMB-R antibodies recognized a band at 80 kDa (predicted 43 kDa); whereas treatment with the deglycosylating agent peptide- N-glycosidase generated bands at 65, 47, and 43 kDa. By immunohistochemistry, both NMB and NMB-R were expressed in normal and cancerous colonic epithelial tissues. In cancer, the amount of NMB was similar to that expressed by proliferating epithelial cells located within the crypt. In contrast, NMB-R expression was increased in cancer, with higher levels detected in better differentiated tumor cells. To assess NMB function, proliferation was determined in the nonmalignant human colonic epithelial cell line NCM-460 and in the colon cancer cell lines Caco-2 and HT-29. Exogenously added NMB was 50–100% more efficacious than gastrin-releasing peptide in causing tumor cell proliferation, whereas only NMB increased NCM-460 cell proliferation. These findings indicate that NMB and its receptor are coexpressed by proliferating cells in which they act in an autocrine fashion with similar and modest potency in both normal and malignant colonic epithelial cells.
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Graziani, Vittoria, Nicoletta Potenza, Brigida D’Abrosca, Teresa Troiani, Stefania Napolitano, Antonio Fiorentino, and Monica Scognamiglio. "NMR Profiling of Ononis diffusa Identifies Cytotoxic Compounds against Cetuximab-Resistant Colon Cancer Cell Lines." Molecules 26, no. 11 (May 28, 2021): 3266. http://dx.doi.org/10.3390/molecules26113266.

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In the search of new natural products to be explored as possible anticancer drugs, two plant species, namely Ononis diffusa and Ononis variegata, were screened against colorectal cancer cell lines. The cytotoxic activity of the crude extracts was tested on a panel of colon cancer cell models including cetuximab-sensitive (Caco-2, GEO, SW48), intrinsic (HT-29 and HCT-116), and acquired (GEO-CR, SW48-CR) cetuximab-resistant cell lines. Ononis diffusa showed remarkable cytotoxic activity, especially on the cetuximab-resistant cell lines. The active extract composition was determined by NMR analysis. Given its complexity, a partial purification was then carried out. The fractions obtained were again tested for their biological activity and their metabolite content was determined by 1D and 2D NMR analysis. The study led to the identification of a fraction enriched in oxylipins that showed a 92% growth inhibition of the HT-29 cell line at a concentration of 50 µg/mL.
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Wang, Rui, In-Kiu Kwon, Muthusamy Thangaraju, Nagendra Singh, Kebin Liu, Philippe Jay, Franz Hofmann, Vadivel Ganapathy, and Darren D. Browning. "Type 2 cGMP-dependent protein kinase regulates proliferation and differentiation in the colonic mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 2 (July 15, 2012): G209—G219. http://dx.doi.org/10.1152/ajpgi.00500.2011.

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Signaling through cGMP has emerged as an important regulator of tissue homeostasis in the gastrointestinal tract, but the mechanism is not known. Type 2 cGMP-dependent protein kinase (PKG2) is a major cGMP effector in the gut epithelium, and the present studies have tested its importance in the regulation of proliferation and differentiation in the mouse colon and in colon cancer cell lines. Tissue homeostasis was examined in the proximal colon of Prkg2 −/− mice using histological markers of proliferation and differentiation. The effect of ectopic PKG2 on proliferation and differentiation was tested in vitro using inducible colon cancer cell lines. PCR and luciferase reporter assays were used to determine the importance of Sox9 downstream of PKG2. The colons of Prkg2 −/− mice exhibited crypt hyperplasia, increased epithelial apoptosis, and reduced numbers of differentiated goblet and enteroendocrine cells. Ectopic PKG2 was able to inhibit proliferation and induce Muc2 and CDX2 expression in colon cancer cells, but did not significantly affect cell death. PKG2 reduced Sox9 levels and signaling, suggesting possible involvement of this pathway downstream of cGMP in the colon. The work presented here demonstrates a novel antiproliferative and prodifferentiation role for PKG2 in the colon. These homeostatic functions of PKG2 were reproducible in colon cancer cells lines where downregulation of Sox9 is a possible mechanism. The similarities in phenotype between PKG2 and GCC knockout mice positions PKG2 as a likely mediator of the homeostatic effects of cGMP signaling in the colon.
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Kilanczyk, Ewa, Urszula Wasik, and Anna Filipek. "CacyBP/SIP phosphatase activity in neuroblastoma NB2a and colon cancer HCT116 cells." Biochemistry and Cell Biology 90, no. 4 (August 2012): 558–64. http://dx.doi.org/10.1139/o2012-011.

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Recently, we have reported that CacyBP/SIP could be a novel phosphatase for ERK1/2 kinase. In this work, we analyzed the CacyBP/SIP phosphatase activity toward ERK1/2 in 2 cell lines of different origin. We showed that overexpression of CacyBP/SIP in NB2a cells resulted in a lower level of phosphorylated ERK1/2 (P-ERK1/2) in the nuclear fraction while such overexpression in HCT116 cells had no effect on the level of P-ERK1/2. Moreover, we found that overexpression of CacyBP/SIP resulted in higher phosphatase activity in the nuclear fraction obtained from NB2a cells when compared with HCT116 cells. Using 2-D electrophoresis we showed that the pattern of spots representing CacyBP/SIP differed in these 2 cell lines and was probably due to a different phosphorylation state of this protein. We also established that after overexpression of CacyBP/SIP in NB2a cells, the amount of nuclear β-catenin was low, while it remained high in HCT116 cells. Since NB2a cells have differentiation potential and HCT116 cells do not, our data suggest that different activity of CacyBP/SIP in these 2 cell lines might affect the ERK1/2 pathway in the differentiation or proliferation processes.
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Bravard, A., J. Beaumatin, E. Dussaulx, T. Lesuffleur, A. Zweibaum, and C. Luccioni. "Modifications of the anti-oxidant metabolism during proliferation and differentiation of colon tumor cell lines." International Journal of Cancer 59, no. 6 (December 15, 1994): 843–47. http://dx.doi.org/10.1002/ijc.2910590622.

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Jordinson, M., I. El-Hariry, D. Calnan, J. Calam, and M. Pignatelli. "Vicia faba agglutinin, the lectin present in broad beans, stimulates differentiation of undifferentiated colon cancer cells." Gut 44, no. 5 (May 1, 1999): 709–14. http://dx.doi.org/10.1136/gut.44.5.709.

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BACKGROUNDDietary lectins can alter the proliferation of colonic cells. Differentiation is regulated by adhesion molecules which, being glycosylated, are targets for lectin binding.AIMSTo examine the effects of dietary lectins on differentiation, adhesion, and proliferation of colorectal cancer cells. METHODSDifferentiation was assessed in three dimensional gels, adhesion by aggregation assay, and proliferation by 3H thymidine incorporation. The role of the epithelial cell adhesion molecule (epCAM) was studied using a specific monoclonal antibody in blocking studies and Western blots. The human colon cancer cell lines LS174T, SW1222, and HT29 were studied.RESULTSThe cell line LS174T differentiated in the presence of Vicia fabaagglutinin (VFA) into gland like structures. This was inhibited by anti-epCAM monoclonal antibody. Expression of epCAM itself was unaffected. VFA as well as wheat germ agglutinin (WGA) and the edible mushroom lectin (Agaricus bisporus lectin, ABL) significantly aggregated LS174T cells but peanut agglutinin (PNA) and soybean agglutinin (SBA) did not. All lectins aggregated SW1222 and HT29 cells. Aggregation was blocked by the corresponding sugars. Aggregation of cells by VFA was also inhibited by anti-epCAM. VFA, ABL, and WGL inhibited proliferation of all the cell lines; PNA stimulated proliferation of HT29 and SW1222 cells. In competition studies all sugars blocked aggregation and proliferation of all cell lines, except that the addition of mannose alone inhibited proliferation.CONCLUSIONVFA stimulated an undifferentiated colon cancer cell line to differentiate into gland like structures. The adhesion molecule epCAM is involved in this. Dietary or therapeutic VFA may slow progression of colon cancer.
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Abu Almaaty, Ali H., Eslam E. M. Toson, El-Sherbiny H. El-Sayed, Mohamed A. M. Tantawy, Eman Fayad, Ola A. Abu Ali, and Islam Zaki. "5-Aryl-1-Arylideneamino-1H-Imidazole-2(3H)-Thiones: Synthesis and In Vitro Anticancer Evaluation." Molecules 26, no. 6 (March 18, 2021): 1706. http://dx.doi.org/10.3390/molecules26061706.

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A novel series of N-1 arylidene amino imidazole-2-thiones were synthesized, identified using IR, 1H-NMR, and 13C-NMR spectral data. Cytotoxic effect of the prepared compounds was carried out utilizing three cancer cell lines; MCF-7 breast cancer, HepG2 liver cancer, and HCT-116 colon cancer cell lines. Imidazole derivative 5 was the most potent of all against three cell lines. DNA flow cytometric analysis showed that, imidazoles 4d and 5 exhibit pre-G1 apoptosis and cell cycle arrest at G2/M phase. The results of the VEGFR-2 and B-Raf kinase inhibition assay revealed that compounds 4d and 5 displayed good inhibitory activity compared with reference drug erlotinib.
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Kato, Masashi, Tomomi Kusumi, Shigeki Tsuchida, Masanori Tanaka, Mutsuo Sasaki, and Hajime Kudo. "Induction of differentiation and peroxisome proliferator-activated receptor ? expression in colon cancer cell lines by troglitazone." Journal of Cancer Research and Clinical Oncology 130, no. 2 (February 1, 2004): 73–79. http://dx.doi.org/10.1007/s00432-003-0510-2.

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Wagner, Hans E., Carol Ann Toth, Glenn D. Steele, and Peter Thomas. "Metastatic potential of human colon cancer cell lines: relationship to cellular differentiation and carcinoembryonic antigen production." Clinical & Experimental Metastasis 10, no. 1 (January 1992): 25–31. http://dx.doi.org/10.1007/bf00163573.

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Dissertations / Theses on the topic "Cancer, differentiation, NMR, colon cell lines"

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Rekas, Agata. "Application of Magnetic Resonance Spectroscopy in Tumor Pathology." University of Sydney, Institute for Magnetic Resonance Research, 1999. http://hdl.handle.net/2123/406.

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Books on the topic "Cancer, differentiation, NMR, colon cell lines"

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United States. National Aeronautics and Space Administration., ed. Morphological differentiation of colon carcinoma cell lines in rotating wall vessels. [Washington, DC: National Aeronautics and Space Administration, 1994.

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