A novel histone deacetylase inhibitor Chidamide induces apoptosis of human colon cancer cells

Liu, Lin; Chen, Baoan; Qin, Shukui; Li, Suyi; He, Xiangming; Shao-min, Qiu; Zhao, Wei; Zhao, Hong

doi:10.1016/j.bbrc.2010.01.011

Cited by 65 publications

(72 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mechanism of the antitumor effect of Chidamide has not yet been clarified. Liu et al showed that Chidamide increased the accumulation of acetylated histone H3 in colon cancer cells (10). Alternatively, it also increased the acetylation levels of non-histone protein.…”

Section: Discussionmentioning

confidence: 99%

“…U937 cells stably expressing ectopic Bcl-2 or Bcl-XL significantly protected cells from MS-275-induced death. Liu et al reported that Chidamide-treated colon cancer cells exhibited swollen mitochondria and increased cleavage of caspase-3 and PARP (10). It is supposed that the mitochondrial-mediated pathway also plays a critical role in apoptosis caused by Chidamide, but the mechanism requires investigation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Antitumor activity of Chidamide in hepatocellular carcinoma cell lines

Wang

Guo

et al. 2012

Mol Med Report

View full text Add to dashboard Cite

Abstract. Chidamide, the structural analog of MS-275, is a novel and promising histone deacetylase (HDAC) inhibitor for use in cancer therapy. To investigate its effects on cancer cell growth, MTT assay was performed in 10 human cancer cell lines. The data showed that the IC 50 of Chidamide ranged from 1 to 13 µM, which was comparable to that of MS-275 in half of the tested cell lines. Furthermore, the growth curve indicated that cell growth was gradually inhibited with an increase in Chidamide dosage, and the inhibition was reversed after drug removal in two hepatocelluclar carcinoma cell lines, BEL-7402 and HCC-9204. To determine cell cycle and apoptosis, FACS was carried out in the BEL-7402 and HCC-9204 cells treated with Chidamide. A decrease in the cell population at S phase and an increase in the cell population at G1 phase occurred in a dose-dependent manner. In addition, Chidamide induced apoptosis and up-regulated p21 mRNA expression. These results suggest that Chidamide may arrest the cell cycle and inhibit the growth of hepatocellular carcinoma cells through up-regulation of p21. Further studies are required to clarify the antitumor activity of Chidamide in vivo and its mechanism in anticancer therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Antitumor activity of Chidamide in hepatocellular carcinoma cell lines

Wang

Guo

et al. 2012

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…Clearly, the selectivity and potential therapeutic index of drugs which modify epigenetic processes will be a key concern. However, we do know that targeting the acetylation of histone proteins with histone deacetylase inhibitors is clinically useful in cancer [Liu et al 2010;Paik and Krug, 2010;Takai and Narahara, 2010]. There is also an increasing literature on the clinical potential of these drugs even in inflammatory diseases [Grabiec et al 2010;Halili et al 2009].…”

Section: Where To Next: Genetics and Epigeneticsmentioning

confidence: 99%

Challenges and prospects for pharmacotherapy in functional gastrointestinal disorders

Sanger

Chang

Bountra

et al. 2010

Therap Adv Gastroenterol

View full text Add to dashboard Cite

Functional gastrointestinal disorders, such as irritable bowel syndrome and functional dyspepsia, are complex conditions with multiple factors contributing to their pathophysiology. As a consequence they are difficult to treat and have posed significant challenges to the pharmaceutical industry when trying to develop new and effective treatments. This review provides an overview of these difficulties and how the industry is reshaping its drug developmental strategies. It describes some of the more significant and encouraging advances that have occurred, and discusses how future research might embrace the opportunities provided by advances in genetic and in particular, epigenetic research.

show abstract

“…It has been confirmed that chidamide can increase the acetylation levels of histone H3 and to inhibit the PI3K/Akt and MAPK/Ras signaling pathways, thus resulting in arresting cancer cells at the G1 phase of the cell cycle and promoting apoptosis [24,25]. Chidamide has just been approved by the Chinese Food and Drug Administration for the treatment of patients with recurrent or refractory peripheral T-cell lymphoma (PTCL) in December 2014.…”

Section: Introductionmentioning

confidence: 98%