|Table of Contents|

Xenoestrogen nonylphenol promotes proliferation,migration,and invasion of colorectal cancer cells by upregulating miR-151a

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

Issue:
2024 22
Page:
4220-4227
Research Field:
Publishing date:

Info

Title:
Xenoestrogen nonylphenol promotes proliferation,migration,and invasion of colorectal cancer cells by upregulating miR-151a
Author(s):
ZHANG Nianjie; ZHANG Yuanwei; YIN Shuo; WAN Lei; CHEN Xu; WANG Biao; YANG Xuefeng
Department of Gastrointestinal Surgery,the Second Affiliated Hospital of Zunyi Medical University,Guizhou Zunyi 563000,China.
Keywords:
colorectal cancer; nonylphenol; cell proliferation; invasion and migration; epithelial-mesenchymal transition; miR-151a
PACS:
R735.3
DOI:
10.3969/j.issn.1672-4992.2024.22.002
Abstract:
Objective:To investigate the relationship between effects of xenoestrogen nonylphenol (NP) in promoting the malignant biological behavior of colorectal cancer cells and miR-151a expression.Methods:HCT-116 and COLO205 cells were selected as experimental cells.EdU and Transwell assays were used to verify the effects of NP on cell proliferation,migration,and invasion.RNA sequencing and qPCR were conducted to analyze the effect of NP on cellular miR-151a.TCGA analysis was performed to examine miR-151a expression in colorectal cancer.EdU and Transwell assays were employed to verify the effects of NP combined with miR-151a overexpression or knockdown on cell proliferation,migration,and invasion.Bioinformatics and dual-luciferase experiments were conducted to validate the targeting relationship between miR-151a and FRK.TCGA analysis was performed to assess FRK expression in colorectal cancer.qPCR was used to detect cellular FRK expression,while Western blot was employed to assess the effects of NP combined with miR-151a overexpression or knockdown on cellular FRK,EMT markers,and WNT/β-catenin pathway proteins.Results:Compared to the Control group,NP significantly promoted cell proliferation,migration,and invasion.RNA sequencing and qPCR analysis indicated a significant increase in cellular miR-151a expression with NP treatment (P＜0.01).Bioinformatics analysis and dual-luciferase experiments confirmed miR-151a targeting inhibition of FRK,with miR-151a exhibiting high expression and FRK showing low expression in colorectal cancer.Compared to the Control group,miR-151a overexpression significantly promoted cell proliferation,migration,and invasion,while miR-151a knockdown inhibited these processes (P＜0.01).Compared to the NP group,NP combined with miR-151a overexpression significantly promoted cell proliferation,migration,and invasion,whereas combined miR-151a knockdown exerted inhibitory effects (P＜0.01).Compared to the Control group,both miR-151a overexpression and NP treatment significantly inhibited cellular E-cadherin and FRK protein expression,while significantly promoting N-cadherin,Vimentin,WNT3a,and β-catenin protein expression.Conversely,miR-151a knockdown yielded opposite results (P＜0.01).Compared to the NP group,NP combined with miR-151a overexpression significantly inhibited cellular E-cadherin and FRK protein expression,while significantly promoting N-cadherin,Vimentin,WNT3a,and β-catenin protein expression.Conversely,combined miR-151a knockdown yielded opposite results (P＜0.01).Conclusion:NP promotes colorectal cancer cell EMT,proliferation,migration,and invasion by upregulating miR-151a to target inhibit FRK,with its molecular mechanism associated with the WNT/β-catenin pathway.

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Memo

Memo:
贵州省科技计划项目(编号：黔科合-ZK［2022］一般631);贵州省卫生健康委科技基金(编号：gzwjkj2020-1-099);遵义医科大学第二附属医院硕士启动基金(编号：SQ-2021-14，SQ-2021-15)
Last Update: 1900-01-01