|Table of Contents|

CHMP4C affects NSCLC cell proliferation and apoptosis by regulating the PI3K/AKT signaling pathway

Journal Of Modern Oncology[ISSN:1672-4992/CN:61-1415/R]

Issue:
2024 09
Page:
1580-1588
Research Field:
Publishing date:

Info

Title:
CHMP4C affects NSCLC cell proliferation and apoptosis by regulating the PI3K/AKT signaling pathway
Author(s):
REN Bi12GOU Haocheng3ZHANG Qin12HE Liping12XUE Linfeng12SUN Jinhong2JIANG Li1
1.Department of Respiratory and Critical Care Medicine,Affiliated Hospital of North Sichuan Medical College,Sichuan Nanchong 637000,China;2.North Sichuan Medical College,Sichuan Nanchong 637000,China;3.Department of Otolaryngology,Head and Neck Surgery,Nanchong Central Hospital,the Second Clinical Medical College of North Sichuan Medical College,Sichuan Nanchong 637000,China.
Keywords:
CHMP4CNSCLCPI3K/AKT signaling pathwaycell proliferationapoptosiscisplatin
PACS:
R734.2
DOI:
10.3969/j.issn.1672-4992.2024.09.002
Abstract:
Objective:To investigate the effect of chromatin modifying protein 4C(CHMP4C) on the progression and cisplatin sensitivity of non-small cell lung cancer(NSCLC) and its underlying mechanism.Methods:Immunohistochemistry(IHC) was used to analyze the expression level of CHMP4C in NSCLC tumor tissues and paracancerous tissues.Real-time fluorescence quantitative PCR(RT-qPCR) and Western blot were used to detect the expression levels of CHMP4C in NSCLC cell lines.Moreover,CCK-8 and cell clone assays were used to detect cell proliferation and IC50(half inhibitory concentration,IC50).Cell cycle and apoptosis were analyzed by flow cytometry.Western blot analyses were performed to examine the expression of caspase 3,Bad and the key proteins in the PI3K/AKT pathway.In addition,we used an animal model to further validate the effect of CHMP4C on tumor growth in vivo.Results:CHMP4C was highly expressed in NSCLC tissues and cell lines,and correlated with T stage(P<0.05).Knockdown of CHMP4C inhibited cell proliferation and promoted apoptosis by blocking the S phase of cell cycle(P<0.05).Moreover,it was found that knockdown of CHMP4C inhibited the activation of the PI3K/AKT signaling pathway,however it's activator reversed the effect of CHMP4C knockdown on NSCLC cells(P<0.05).Additionally,treatment of NSCLC cells with cisplatin revealed that cell growth was inhibited and CHMP4C expression was reduced.Cisplatin treatment of CHMP4C knockdown cells significantly induced tumor cell apoptosis and inhibited cell proliferation(P<0.05).In animal experiments,the tumor volume of CHMP4C knockdown group was smaller than the control group,and its ki67 expression was significantly reduced while caspase 3 expression was increased(P<0.05).Conclusion:The expression of CHMP4C in NSCLC tumor tissues and cell lines was increased.Knockdown of CHMP4C in vivo and in vitro inhibited NSCLC cell proliferation,promoted apoptosis,and enhanced the sensitivity of cisplatin to cells.CHMP4C may be involved in NSCLC progression and cisplatin resistance through the PI3K/AKT signaling pathway.

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Memo

Memo:
四川省科技计划项目(编号:2021YFS0572);四川省医学会项目(编号:2021HR24)
Last Update: 2024-03-29