Galangin cooperates with oxaliplatin to inhibit the proliferation and invasion of colorectal cancer cells by targeting CBX3

Author:

Chu Bowei1,Lou Yuanmei1,Yu Qifeng1

Affiliation:

1. Zhoushan Hospital, Wenzhou Medical University

Abstract

Abstract Objective Examining the potential mechanism underlying the effect of galangin combined with oxaliplatin on the invasion and proliferation of colorectal cancer. Methods The effects of galangin combined with oxaliplatin on colorectal cancer (CRC) cell invasion and proliferation were assessed using CCK8 and Transwell assays. Using WB and qPCR, the expression of CBX3 in several CRC cell lines was identified. The levels of CBX3 in normal colorectal tissues and CRC tissues were compared using HPA and GEPIA, and the impact of CBX3 on the prognosis of CRC patients was investigated using GEPIA. To determine whether galangin targets CBX3 to influence the growth and invasion of CRC cells, cell assays were employed. The levels of ROS in HCT116 were measured by immunofluorescence following galangin treatment. The impact of CBX3 on immune cell infiltration in CRC was examined using TIMER. GEPIA produced a list of CBX3-related genes, and R was utilized to perform GO/KEGG enrichment analysis. Results We found that galangin combined with oxaliplatin inhibited the proliferation and invasion of CRC cells and down-regulated the expression of CBX3, which was rescued by overexpression of CBX3. DFS was shorter in those with elevated CBX3 expression. The level of ROS in HCT116 was significantly increased after galangin treatment. The invasion of CD8 + T cells and macrophages in the immunological microenvironment of CRC is favorably linked with increased expression of CBX3. Nuclear chromatin, histone binding, and covalent chromatin modification are enriched regions in CBX3 and related genes. Conclusion Galangin combine with oxaliplatin can inhibit the proliferation and invasion of colorectal cancer cells by down-regulating the expression of CBX3, and CBX3 is highly expressed in colorectal cancer and is related to short DFS.

Publisher

Research Square Platform LLC

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3