Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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Τρίτη 2 Μαΐου 2017

Cisatracurium-induced proliferation impairment and death of colorectal cancer cells, HCT116 is mediated by p53 dependent intrinsic apoptotic pathway in vitro

Publication date: July 2017
Source:Biomedicine & Pharmacotherapy, Volume 91
Author(s): Iddrisu Baba Yabasin, ZhiLi Lu, Jia-Chuan Yu, Qingping Wen
Activation of oncogenes and suppression of repressor genes are believed to play crucial roles in the pathogenesis of human colorectal carcinoma. Cisatracurium, a nondepolarizing neuromuscular blocking agent, has been reported to inhibit cell proliferation while promoting apoptosis. However, the underlining mechanism, of these growth setbacks are not well understood. We assessed the growth of human colorectal carcinoma (HCT116) and its cell cycle distribution upon cisatracurium exposure. Significant cell growth inhibition and accumulation of cells in G1 phase of the cell cycle was observed in treated cells compared with untreated cells (control). In furtherance to these observations, FITC Annexin V and propidium iodide apoptosis assay demonstrated concentration and time dependent percentage increase in apoptosis of cells treated with cisatracurium compared with untreated cells. qRT-PCR analysis showed concentration-dependent alterations in CD1, E2F, CE1, p53 and p21 mRNA expression. Western blot analysis indicated remarkable concentration dependent alterations in the expression of proliferation and survival proteins CD1, E2F, CE1, p53, p21, BAX, BCL-2, cytochrome C and cleaved PARP in cisatracurium-treated groups as compared with the untreated group. Cisatracurium also significantly promoted caspase-9 and caspase-3 activities in cells treated with cisatracurium compared with untreated cells. Thus, cisatracurium effectively inhibited proliferation and induced apoptosis of HCT116 cells in vitro at least via alteration of p53-dependent apoptotic pathway.



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