Colorectal cancer cells with high metastatic potential drive metastasis by transmitting exosomal miR-20a-3p through modulating NF1/MAPK pathway.

IF 3.3 3区医学 Q2 ONCOLOGY

Carcinogenesis Pub Date : 2024-10-10 DOI:10.1093/carcin/bgae036

Yahang Liang, Junyu Li, Tao Li, Mingming Li, Hualin Liao, Yang Liu, Yao Yao, Lingling Yang, Xiong Lei

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引用次数: 0

Abstract

Cancer cells exhibit heterogeneous metastatic potential, and high metastatic (HM) subclones can enhance the metastatic potential of low metastatic subclones by transmitting some factors. Exosomal miRNAs play a pivotal role in the crosstalk of heterogeneous metastatic subclones. This study discovered that miR-20a-3p was upregulated in colorectal adenocarcinoma (CRA), correlated with metastasis, and potentially served as a prognostic indicator for CRA. miR-20a-3p could promote the proliferation, migration, and invasion of CRA cells. Interestingly, HM CRA cells could promote malignant phenotypes of low metastatic CRA cells by transmitting exosomal miR-20a-3p. Mechanically, miR-20a-3p could inhibit neurofibromin 1(NF1), thereby activate the rat sarcoma viral oncogene (RAS)-mediated mitogen-activated protein kinases (MAPK) signaling pathway to drive the metastasis of CRA. In summary, our study provided evidence that colorectal cancer cells with HM potential drive metastasis by transmitting exosomal miR-20a-3p through modulating the NF1/MAPK pathway.

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具有高转移潜能的结直肠癌细胞通过调节 NF1/MAPK 通路传递外泌体 miR-20a-3p 推动转移。

癌细胞具有异源转移潜能，高转移亚克隆可通过传递某些因子增强低转移亚克隆的转移潜能。外泌体 miRNA 在异源转移亚克隆的串联中发挥着关键作用。这项研究发现，miR-20a-3p 在结直肠腺癌（CRA）中上调，并与转移相关，有可能成为 CRA 的预后指标。有趣的是，高转移性CRA细胞可通过传递外泌体miR-20a-3p促进低转移性CRA细胞的恶性表型。从机制上讲，miR-20a-3p 可抑制 NF1，从而激活 RAS 介导的丝裂原活化蛋白激酶（MAPK）信号通路，驱动 CRA 转移。总之，我们的研究提供了证据，证明具有高转移潜能的结直肠癌细胞通过调控NF1/MAPK通路传递外泌体miR-20a-3p来驱动转移。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Carcinogenesis 医学-肿瘤学

CiteScore

9.20

自引率

2.10%

发文量

审稿时长

1 months

期刊介绍： Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).