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Abstract <p>In the serum exosomes of hepatocellular carcinoma (HCC) patients, miR-4661-5p is reported at a high level. This study aimed to investigate the effect of exosomal miR-4661-5p on the malignant progression of HCC and its mechanism of action. Exosomes were separated from SNU387 cells and identified and miR-4661-5p expression were tested using qRT-PCR. CCK-8, clone formation, and Transwell assays tested the biological characteristics of HCC cells, and flow cytometry determined apoptosis rate. Dual-luciferase reporter gene tests verified the targeting connection between miR-4661-5p and Estrogen receptor alpha (ESR1). Moreover, a subcutaneous graft tumor model was constructed in nude mice. MiR-4661-5p exhibited an elevated level in HCC cells and their exosomes; ESR1 exhibited a notably diminished level in HCC cells; miR-4661-5p targeted and negatively regulated ESR1. After co-culturing with exosomes, Hep3B and Huh7 cells showed heightened levels of miR-4661-5p. Exosomal miR-4661-5p promoted the migration and invasion of HCC cells and depressed apoptosis. Overexpression ESR1 partially declined the promoting impact of over-expressed exosomal miR-4661-5p on the proliferation and invasion ability of Hep3B and Huh7 cells and the suppression of apoptosis. In addition, exosomal or over-expressed miR-4661-5p accelerated tumor expansion in nude mice by regulating the level of ESR1. In conclusion, exosomal miR-4661-5p targets and downregulates ESR1, leading to the promotion of HCC malignant progression, identified exosomal miR-4661-5p and ESR1 as potential therapeutic targets for HCC.</p>

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Tumor-Derived Exosome miR-4661-5p Exerts Tumor-Promoting Effects in Hepatocellular Carcinoma by Targeting ESR1

  • 期刊论文

  • 发表日期：

    2025年6月10日

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  • Sha Li,
  • Qian Wang,
  • Lixiu Xu,
  • Mengmeng Liu,
  • Yingguang Ma,
  • Wensheng Liu

摘要

Abstract

In the serum exosomes of hepatocellular carcinoma (HCC) patients, miR-4661-5p is reported at a high level. This study aimed to investigate the effect of exosomal miR-4661-5p on the malignant progression of HCC and its mechanism of action. Exosomes were separated from SNU387 cells and identified and miR-4661-5p expression were tested using qRT-PCR. CCK-8, clone formation, and Transwell assays tested the biological characteristics of HCC cells, and flow cytometry determined apoptosis rate. Dual-luciferase reporter gene tests verified the targeting connection between miR-4661-5p and Estrogen receptor alpha (ESR1). Moreover, a subcutaneous graft tumor model was constructed in nude mice. MiR-4661-5p exhibited an elevated level in HCC cells and their exosomes; ESR1 exhibited a notably diminished level in HCC cells; miR-4661-5p targeted and negatively regulated ESR1. After co-culturing with exosomes, Hep3B and Huh7 cells showed heightened levels of miR-4661-5p. Exosomal miR-4661-5p promoted the migration and invasion of HCC cells and depressed apoptosis. Overexpression ESR1 partially declined the promoting impact of over-expressed exosomal miR-4661-5p on the proliferation and invasion ability of Hep3B and Huh7 cells and the suppression of apoptosis. In addition, exosomal or over-expressed miR-4661-5p accelerated tumor expansion in nude mice by regulating the level of ESR1. In conclusion, exosomal miR-4661-5p targets and downregulates ESR1, leading to the promotion of HCC malignant progression, identified exosomal miR-4661-5p and ESR1 as potential therapeutic targets for HCC.