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<p>This study aimed to explore the expression, biological function, and regulatory mechanism of lncRNA TRHDE‑AS1 in ovarian cancer (OC). The GEO dataset GSE119056 and the GEPIA2 database were used to assess the expression level of TRHDE-AS1 in OC tissues. In vitro experiments, including RT-qPCR, CCK-8, Transwell, and dual-luciferase reporter assays, were performed in SKOV3 and 3AO cells to clarify the biological function of TRHDE-AS1 and its ceRNA regulatory network involving miR-17-5p and PIK3R1. TRHDE-AS1 was downregulated in OC tissues and cell lines. TRHDE-AS1 inhibited the proliferation, migration, and invasion of OC cells. Mechanistically, TRHDE-AS1 was predominantly localized in the cytoplasm and directly bound to miR-17-5p. miR-17-5p targeted the 3’UTR of PIK3R1 and negatively regulates its expression. TRHDE‑AS1 upregulated PIK3R1 expression by sponging miR‑17‑5p. Functional rescue assays confirmed that miR‑17‑5p mimic reversed the tumor‑suppressive effects of TRHDE‑AS1 overexpression, while PIK3R1 overexpression restored these inhibitory effects. TRHDE-AS1 functions as a tumor suppressor in OC by regulating the miR-17-5p/PIK3R1 axis, which provides a potential molecular target for OC targeted therapy.</p>

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LncRNA TRHDE-AS1 functions as a tumor suppressor in ovarian cancer via the miR-17-5p/PIK3R1 ceRNA regulatory axis

  • 期刊论文

  • 发表日期：

    2026年7月16日

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  • Hui Liu,
  • Chengwen Song,
  • Dan Cheng,
  • Jianhua Sun,
  • Chuchao Zhu,
  • Yuan Huang

摘要

This study aimed to explore the expression, biological function, and regulatory mechanism of lncRNA TRHDE‑AS1 in ovarian cancer (OC). The GEO dataset GSE119056 and the GEPIA2 database were used to assess the expression level of TRHDE-AS1 in OC tissues. In vitro experiments, including RT-qPCR, CCK-8, Transwell, and dual-luciferase reporter assays, were performed in SKOV3 and 3AO cells to clarify the biological function of TRHDE-AS1 and its ceRNA regulatory network involving miR-17-5p and PIK3R1. TRHDE-AS1 was downregulated in OC tissues and cell lines. TRHDE-AS1 inhibited the proliferation, migration, and invasion of OC cells. Mechanistically, TRHDE-AS1 was predominantly localized in the cytoplasm and directly bound to miR-17-5p. miR-17-5p targeted the 3’UTR of PIK3R1 and negatively regulates its expression. TRHDE‑AS1 upregulated PIK3R1 expression by sponging miR‑17‑5p. Functional rescue assays confirmed that miR‑17‑5p mimic reversed the tumor‑suppressive effects of TRHDE‑AS1 overexpression, while PIK3R1 overexpression restored these inhibitory effects. TRHDE-AS1 functions as a tumor suppressor in OC by regulating the miR-17-5p/PIK3R1 axis, which provides a potential molecular target for OC targeted therapy.