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<p>The aim of this study was to explore the role of microRNA-767-5p (miR-767-5p) in regulating the osteosarcoma (OS) prognosis, metastasis and sensitivity to chemotherapeutic and radiotherapeutic sensitivity. We observed that miR-767-5p expression in the specimens of patients with metastatic OS was higher than in healthy individuals and was also negatively correlated with the overall survival of patients with OS. Functional assays (CCK-8, transwell, colony formation) and a tumor xenograft model demonstrated that miR-767-5p over-expression in both U2OS and 143B OS cell lines promoted cell invasion and migration without affecting proliferation, whereas its knockdown had opposite effects. Notably, miR-767-5p over-expression enhanced the sensitivity of both U2OS and 143B cells to chemotherapy or radiotherapy. Combing target gene prediction, RNA-sequencing and overall survival analysis, we identified aryl hydrocarbon receptor (AHR) as the potential target gene of miR-767-5p. Luciferase assay confirmed that miR-767-5p promoted the 3’-UTR activity of AHR through direct binding. Strikingly, AHR over-expression in both U2OS and 143B cells suppressed invasion, migration while reduced therapeutic sensitivity to chemotherapy and radiotherapy—thereby reversing miR-767-5p’s phenotypic impact. Therefore, this study suggested that miR-767-5p promotes OS metastasis but improves its sensitivity to radiotherapy and chemotherapy.</p>

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MicroRNA-767-5p promotes metastasis but improves chemotherapeutic and radiotherapeutic sensitivity of osteosarcoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月15日

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  • Xuelian Luo,
  • Xiaoyan Dai,
  • Qingsong Wei,
  • Xiaorong Tan,
  • Shuai Wang,
  • Hanxi Xiao,
  • Xuan Yao,
  • Youcai Deng,
  • Zhaoyang Zhong

摘要

The aim of this study was to explore the role of microRNA-767-5p (miR-767-5p) in regulating the osteosarcoma (OS) prognosis, metastasis and sensitivity to chemotherapeutic and radiotherapeutic sensitivity. We observed that miR-767-5p expression in the specimens of patients with metastatic OS was higher than in healthy individuals and was also negatively correlated with the overall survival of patients with OS. Functional assays (CCK-8, transwell, colony formation) and a tumor xenograft model demonstrated that miR-767-5p over-expression in both U2OS and 143B OS cell lines promoted cell invasion and migration without affecting proliferation, whereas its knockdown had opposite effects. Notably, miR-767-5p over-expression enhanced the sensitivity of both U2OS and 143B cells to chemotherapy or radiotherapy. Combing target gene prediction, RNA-sequencing and overall survival analysis, we identified aryl hydrocarbon receptor (AHR) as the potential target gene of miR-767-5p. Luciferase assay confirmed that miR-767-5p promoted the 3’-UTR activity of AHR through direct binding. Strikingly, AHR over-expression in both U2OS and 143B cells suppressed invasion, migration while reduced therapeutic sensitivity to chemotherapy and radiotherapy—thereby reversing miR-767-5p’s phenotypic impact. Therefore, this study suggested that miR-767-5p promotes OS metastasis but improves its sensitivity to radiotherapy and chemotherapy.