scholarly journals THE INHIBITION OF POLYISOPRENOIDS FROM NYPA FRUTICANS LEAVES ON CYCLOOXYGENASE 2 EXPRESSION OF WIDR COLON CANCER CELLS

2018 ◽  
Vol 11 (8) ◽  
pp. 154 ◽  
Author(s):  
Dini Permata Sari ◽  
Mohammad Basyuni ◽  
Poppy Anjelisa Zaitun Hasibuan ◽  
Ridha Wati
Keyword(s):  
Colon Cancer ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Colon Cancer Cell ◽  
Cyclooxygenase 2 ◽  
Colon Cancer Cells ◽  
Chemopreventive Agents ◽  
Nypa Fruticans ◽  
Diphenyltetrazolium Bromide ◽  
Cox 2

Objective: The objective of the study was to investigate the inhibitory activity of polyisoprenoids from Nypa fruticans leaves on the expression of cyclooxygenase 2 (COX-2) against colon cancer cells.Methods: Anticancer activity performed was tested by dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method on colon cancer cell WiDr. The expression of COX-2 was observed by the immunocytochemistry method.Result: Polyisoprenoids from N. fruticans leaves exhibit anticancer activity on WiDr cells through inhibition of COX-2 expression with IC50 180.186±7.16 μg/ml.Conclusions: This study showed that polyisoprenoids from N. fruticans leaves promise chemopreventive agents for colon cancer through COX-2 inhibition.

scholarly journals Cyclooxygenase-2 Regulation in Colon Cancer Cells

2005 ◽  
Vol 280 (16) ◽  
pp. 15503-15509 ◽  
Author(s):  
Xin Tong ◽  
Lei Yin ◽  
Shree Joshi ◽  
Daniel W. Rosenberg ◽  
Charles Giardina
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Histone Deacetylase Inhibitors ◽  
Trichostatin A ◽  
Cancer Cell Line ◽  
Cyclooxygenase 2 ◽  
Pharmacological Intervention ◽  
Colon Cancer Cells ◽  
Tnf Α ◽  
Cox 2

We are interested in the mechanism of cyclooxygenase-2 (Cox-2) regulation in colon cancer cells because this knowledge could provide insight into colon carcinogenesis and suggest ways to suppress Cox-2 expression in colon tumors. Studying the HT-29 colon cancer cell line as a model, we found that Cox-2 mRNA and protein levels were activated over 10-fold by the inflammatory cytokine tumor necrosis factor (TNF)-α. Moreover, we found that the histone deacetylase inhibitors butyrate and trichostatin A could block Cox-2 activation in a gene-specific manner. TNF-α and butyrate did not significantly affect Cox-2 promoter activity, mRNA stability, or negative regulation by the Cox-2 3′-untranslated RNA region. A nuclear run-on assay showed that TNF-α increased Cox-2 transcription, whereas butyrate was suppressive. Because butyrate has been reported to suppress polymerase elongation on the c-mycgene, we employed the chromatin immunoprecipitation assay to determine the influence of butyrate and trichostatin A on polymerase distribution on the Cox-2 gene. These data indicated that butyrate restricted polymerase elongation from exon 1 to 2 on both the c-mycand Cox-2 genes. We propose that histone deacetylases regulate a transcriptional block on the Cox-2 and c-mycgenes and that this block may be a potential target for pharmacological intervention.

scholarly journals POTENTIATION OF THE CYTOTOXIC ACTIVITY OF MELOXICAM AGAINST COX-2 NEGATIVE COLON CANCER CELLS BY NANOPARTICULATE ENCAPSULATION

2019 ◽  
Vol 11 ◽  
pp. 9
Author(s):  
Areeg Awadallah ◽  
Keyword(s):  
Colon Cancer ◽  
Cytotoxic Activity ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Current Work ◽  
Colon Cancer Cells ◽  
Cox 2

The aim of the current work was to elucidate whether the nanoencapsulation of meloxicam would allow its exertion of anticancer activity on colon cancer cells despite lacking COX-2 expression.

scholarly journals CXCL2-CXCR2 axis mediates αV integrin-dependent peritoneal metastasis of colon cancer cells

2021 ◽  
Author(s):  
Mattias Lepsenyi ◽  
Nader Algethami ◽  
Amr A. Al-Haidari ◽  
Anwar Algaber ◽  
Ingvar Syk ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Cancer Cell Adhesion ◽  
And Migration ◽  
Cxcr2 Antagonist

AbstractPeritoneal metastasis is an insidious aspect of colorectal cancer. The aim of the present study was to define mechanisms regulating colon cancer cell adhesion and spread to peritoneal wounds after abdominal surgery. Mice was laparotomized and injected intraperitoneally with CT-26 colon carcinoma cells and metastatic noduli in the peritoneal cavity was quantified after treatment with a CXCR2 antagonist or integrin-αV-antibody. CT-26 cells expressed cell surface chemokine receptors CXCR2, CXCR3, CXCR4 and CXCR5. Stimulation with the CXCR2 ligand, CXCL2, dose-dependently increased proliferation and migration of CT-26 cells in vitro. The CXCR2 antagonist, SB225002, dose-dependently decreased CXCL2-induced proliferation and migration of colon cancer cells in vitro. Intraperitoneal administration of CT-26 colon cancer cells resulted in wide-spread growth of metastatic nodules at the peritoneal surface of laparotomized animals. Laparotomy increased gene expression of CXCL2 at the incisional line. Pretreatment with CXCR2 antagonist reduced metastatic nodules by 70%. Moreover, stimulation with CXCL2 increased CT-26 cell adhesion to extracellular matrix (ECM) proteins in a CXCR2-dependent manner. CT-26 cells expressed the αV, β1 and β3 integrin subunits and immunoneutralization of αV abolished CXCL2-triggered adhesion of CT-26 to vitronectin, fibronectin and fibrinogen. Finally, inhibition of the αV integrin significantly attenuated the number of carcinomatosis nodules by 69% in laparotomized mice. These results were validated by use of the human colon cancer cell line HT-29 in vitro. Our data show that colon cancer cell adhesion and growth on peritoneal wound sites is mediated by a CXCL2-CXCR2 signaling axis and αV integrin-dependent adhesion to ECM proteins.

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