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Updated: Feb 16, 2026

Multi-photon Imaging of Tumor Cell Invasion in an Orthotopic Mouse Model of Oral Squamous Cell Carcinoma
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Multi-photon Imaging of Tumor Cell Invasion in an Orthotopic Mouse Model of Oral Squamous Cell Carcinoma

Published on: July 25, 2011

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Function of miR‑152 as tumor suppressor in oral squamous cell carcinoma cells by targeting c‑MET

Minghe Li1, Zhihong Li2, Xue Wang3

  • 1Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, Jilin University, Changchun, Jilin 130021, P.R. China.

Oncology Reports
|December 30, 2017
PubMed

Insights

MicroRNA-152 (miR-152) acts as a tumor suppressor in oral squamous cell carcinoma (OSCC). Restoring miR-152 inhibits OSCC progression by targeting c-MET, offering a potential therapeutic strategy for this cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNA-152 (miR-152) involvement in cancer is known, but its role in oral squamous cell carcinoma (OSCC) is unclear.
  • Understanding miR-152's function and regulation in OSCC is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the expression, function, and mechanism of miR-152 in oral squamous cell carcinoma (OSCC).
  • To determine if miR-152 acts as a tumor suppressor in OSCC and identify its molecular targets.

Main Methods:

  • Analysis of miR-152 expression in OSCC cell lines and tissues.
  • In vitro experiments assessing the effects of miR-152 restoration on OSCC cell proliferation, migration, and invasion.
  • Investigation of miR-152's interaction with c-MET and its downstream PI3K/AKT pathway.
  • In vivo studies using xenograft mouse models to evaluate miR-152's effect on tumor growth.

Main Results:

  • miR-152 was significantly downregulated in OSCC tissues and cell lines, correlating with poor patient survival and lymph node metastasis.
  • Restoring miR-152 suppressed OSCC cell proliferation, colony formation, migration, and invasion.
  • miR-152 directly targeted cellular-mesenchymal to epithelial transition factor (c-MET), downregulating its expression and the PI3K/AKT pathway.
  • In vivo, miR-152 restoration inhibited tumor growth by repressing c-MET.

Conclusions:

  • miR-152 functions as a tumor suppressor in oral squamous cell carcinoma (OSCC).
  • The tumor-suppressive role of miR-152 is mediated through direct targeting of c-MET and inhibition of the PI3K/AKT pathway.
  • miR-152 represents a promising therapeutic target for oral squamous cell carcinoma.

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