We have located links that may give you full text access.
Cisatracurium-induced proliferation impairment and death of colorectal cancer cells, HCT116 is mediated by p53 dependent intrinsic apoptotic pathway in vitro.
Biomedicine & Pharmacotherapy 2017 July
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.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app