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MicroRNA-433 inhibits oral squamous cell carcinoma cells by targeting FAK

Yong-Jian Wang1, Zi-Feng Zhang1, Shao-Hua Fan1

  • 1Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.

Oncotarget
|December 17, 2017
PubMed

Insights

MicroRNA-433 (miR-433) inhibits oral squamous cell carcinoma (OSCC) growth by downregulating focal adhesion kinase (FAK) via the ERK/MAPK pathway. This finding offers potential therapeutic targets for OSCC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Oral squamous cell carcinoma (OSCC) is a prevalent malignancy with complex regulatory mechanisms.
  • MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
  • Identifying key molecular players like miR-433 is vital for understanding OSCC pathogenesis.

Purpose of the Study:

  • To investigate the role of microRNA-433 (miR-433) in the proliferation, migration, and invasiveness of oral squamous cell carcinoma (OSCC).
  • To elucidate the molecular mechanism by which miR-433 influences OSCC progression, focusing on the focal adhesion kinase (FAK)/ERK/MAPK signaling pathway.
  • To assess the therapeutic potential of modulating miR-433 in OSCC.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting to measure miRNA and protein expression levels.
  • Cellular assays including flow cytometry, MTT assay, scratch test, and Transwell assay to evaluate cell proliferation, migration, and invasion.
  • In vivo studies using a subcutaneous transplanted tumor model in nude mice to assess the effect of miR-433 and FAK.
  • Transfection of SCC-9 cells with miR-433 mimics, inhibitors, and small interfering RNA (siFAK) to manipulate gene expression.

Main Results:

  • miR-433 expression was elevated in OSCC tissues and miR-433 mimics reduced OSCC cell proliferation, migration, and invasion.
  • miR-433 mimics decreased the expression of FAK, ERK, MEK, p-ERK, and p-MEK, while miR-433 inhibitors showed opposite effects.
  • Downregulation of FAK by miR-433 occurred through the ERK/MAPK signaling pathway, inhibiting tumor stem cell characteristics and subcutaneous tumor formation.
  • CD44+ cells exhibited characteristics of tumor stem cells, and FAK, ERK, MEK, p-ERK, and p-MEK were decreased in CD44-, miR-433, and siFAK groups.

Conclusions:

  • miR-433 acts as a tumor suppressor in OSCC by inhibiting proliferation, migration, and invasiveness.
  • miR-433 exerts its effects by downregulating FAK expression through the ERK/MAPK signaling pathway.
  • Modulating miR-433 and FAK represents a potential therapeutic strategy for OSCC.
Keywords:
ERKFAKSCC-9 cellmicroRNA-433oral squamous cell carcinoma

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