TCF3-activated LINC00152 exerts oncogenic role in osteosarcoma through regulating miR-1182/CDK14 axis

Longlong Zheng1, Nan Hu2, Xiaozhong Zhou3

  • 1Department of Orthopedics, The Second Affiliated Hospital of Suzhou University, Suzhou, Jiangsu, 215008, China; Department of Orthopedics, Chuzhou Medical College of Anhui Medical University, Chuzhou, Anhui, 239000, China.

Insights

Long noncoding RNA LINC00152 promotes osteosarcoma progression. This study reveals LINC00152, activated by TCF3, drives cancer cell proliferation and migration via the miR-1182/CDK14 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in cancer development.
  • The specific role of lncRNA LINC00152 in osteosarcoma (OS) is not well understood.

Purpose of the Study:

  • To investigate the function and mechanism of lncRNA LINC00152 in osteosarcoma.
  • To elucidate the regulatory pathway involving LINC00152, TCF3, and the miR-1182/CDK14 axis in OS.

Main Methods:

  • Quantitative analysis of LINC00152 expression in OS tissues and cell lines.
  • Cell proliferation assays (MTT, colony formation) and migration/invasion assays (Transwell).
  • Chromatin immunoprecipitation (ChIP), luciferase reporter assays, and mechanistic studies to identify regulatory interactions.

Main Results:

  • LINC00152 expression is significantly upregulated in osteosarcoma.
  • Knockdown of LINC00152 inhibits osteosarcoma cell proliferation, migration, and invasion.
  • LINC00152 is transcriptionally activated by TCF3 and functions as a competing endogenous RNA (ceRNA) by sponging miR-1182, thereby upregulating CDK14.

Conclusions:

  • LINC00152 plays a crucial oncogenic role in osteosarcoma.
  • TCF3-induced LINC00152 promotes osteosarcoma progression through the LINC00152/miR-1182/CDK14 axis.

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