scholarly journals Leptin Counteracts Sodium Butyrate-induced Apoptosis in Human Colon Cancer HT-29 Cells via NF-κB Signaling

2004 ◽  
Vol 279 (16) ◽  
pp. 16495-16502 ◽  
Author(s):  
Patricia Rouet-Benzineb ◽  
Thomas Aparicio ◽  
Sandra Guilmeau ◽  
Cécile Pouzet ◽  
Véronique Descatoire ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Sodium Butyrate ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Induced Apoptosis ◽  
Ht 29

Sodium Butyrate Induces Human Colon Carcinoma HT-29 Cell Apoptosis through a Mitochondrial Pathway

2009 ◽  
Vol 37 (3) ◽  
pp. 803-811 ◽  
Author(s):  
L Wang ◽  
H-S Luo ◽  
H Xia
Keyword(s):  
Colon Cancer ◽  
Sodium Butyrate ◽  
Caspase 3 ◽  
Cancer Cell Line ◽  
Human Colon ◽  
Caspase 9 ◽  
Human Colon Cancer ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ht 29

Some tumours respond favourably to tumour necrosis factor-alpha (TNF-α). Despite this preferential sensitivity, resistance to TNF-α remains a clinical problem and more interest is now being focused on finding compounds that induce apoptosis through other pathways. Sodium butyrate (NaBt) has anti-tumour effects on colon cancer cells, inhibiting cell growth and promoting differentiation and apoptosis. In this study we investigated whether NaBt induced apoptosis in the human colon cancer cell line HT-29 and examined the intracellular mechanisms involved. Pre-incubation of cells with NaBt significantly increased apoptosis as measured by fluorescence activated cell sorter analysis and mitochondrial membrane potential determination. This effect could be blocked with the caspase inhibitors, z-VAD-fmk (pan-caspase inhibitor), z-DEVD-fmk (caspase-3 inhibitor) and z-LEHD-fmk (caspase-9 inhibitor), but not with z-IETD-fmk (caspase-8 inhibitor). Enhancement of caspase-3 and caspase-9 activities suggests that NaBt induces apoptosis via mitochondrial pathways not involving TNF-α.

scholarly journals Activation of caspase‐8 contributes to fucoidan‐induced apoptosis in HT‐29 human colon cancer cells

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Eun Ji Kim ◽  
So Young Park ◽  
Hee Sook Park ◽  
Ji Eun Hong ◽  
Min Jeong Sin ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Caspase 8 ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Induced Apoptosis ◽  
Human Colon Cancer Cells ◽  
Ht 29

Mechanisms of thiosulfinates from Allium tuberosum L.-induced apoptosis in HT-29 human colon cancer cells

2009 ◽  
Vol 188 (2) ◽  
pp. 142-147 ◽  
Author(s):  
Ju-Hye Lee ◽  
Hee-Sun Yang ◽  
Kyoung-Wuk Park ◽  
Jae-Yong Kim ◽  
Mi-Kyung Lee ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Allium Tuberosum ◽  
Induced Apoptosis ◽  
Human Colon Cancer Cells ◽  
Ht 29

Upregulation of activin A gene by butyrate in human colon cancer cell lines

2003 ◽  
Vol 284 (6) ◽  
pp. G989-G995 ◽  
Author(s):  
Kei Sonoyama ◽  
Pimara Pholnukulkit ◽  
Masahiko Toyoda ◽  
Suriya Rutatip ◽  
Takanori Kasai
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Sodium Butyrate ◽  
Human Colon ◽  
Activin A ◽  
Human Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines ◽  
Ht 29

Activin A has been reported to play a role in the progression of colorectal cancer. Because dietary fiber protects against colorectal cancer, we hypothesized that butyrate, a fermentation product of dietary fiber, may affect the expression of activin A in colon cancer cells. Semiquantitative RT-PCR demonstrated that the activin A gene was upregulated by sodium butyrate in the human colon cancer cell lines HT-29 and Caco-2 in a concentration- and time-dependent manner. However, the activin A gene did not respond to sodium butyrate in the human normal colonic cell line FHC, rat normal intestinal epithelial cell (IEC) line IEC-6, and the explant of rat colon. Flow cytometry and agarose gel electrophoresis of genomic DNA revealed that cell cycle arrest and apoptosis were induced by sodium butyrate but not exogenous activin A in HT-29 cells, indicating that activin A could not act as an autocrine factor in colon cancer cells. By assuming that activin A promotes colorectal cancer spread as a paracrine factor, our findings suggest that butyrate could act as a tumor promoter in some circumstances.

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