miR-494 inhibits cervical cancer cell proliferation through upregulation of SOCS6 expression

Lei Cheng1,2, Beihua Kong1, Ying Zhao2

  • 1Department of Obstetrics and Gynecology, Qi Lu Hospital of Shandong University Jinan, Jinan, Shandong 250012, P.R. China.

Oncology Letters
|February 20, 2018
PubMed

Insights

MicroRNA (miR)-494 is significantly decreased in cervical cancer, inhibiting cancer cell proliferation and invasion by upregulating suppressor of cytokine signaling 6 (SOCS6). This finding clarifies the molecular mechanism of miR-494 in cervical cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cervical cancer remains a significant global health challenge.
  • The precise molecular mechanisms by which microRNAs regulate cancer progression are not fully understood.
  • MicroRNA-494 (miR-494) has been implicated in various cancers, but its role in cervical cancer requires further elucidation.

Purpose of the Study:

  • To investigate the molecular mechanism of miR-494 in regulating the expression of suppressor of cytokine signaling 6 (SOCS6) in cervical cancer.
  • To determine the effect of miR-494 on the proliferation and invasion of human cervical cancer cells.
  • To correlate miR-494 expression levels with clinical parameters in cervical cancer patients.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (RT-qPCR) for miR-494 expression analysis.
  • Bioinformatic prediction (TargetScan) and luciferase reporter assays to validate miR-494 targeting of SOCS6.
  • In vitro assays including MTT and Boyden chamber assays to assess cell proliferation and invasion.
  • Western blot analysis to evaluate SOCS6 protein expression.

Main Results:

  • miR-494 expression was significantly decreased in cervical cancer tissues compared to normal and pre-cancerous tissues.
  • Decreased miR-494 expression correlated with lymph node metastasis, clinical stage, and stromal invasion depth.
  • miR-494 mimic transfection inhibited proliferation and invasion of HeLa cells, while anti-miR-494 transfection enhanced these abilities.
  • SOCS6 was confirmed as a direct target of miR-494, and miR-494 upregulation led to increased SOCS6 expression.

Conclusions:

  • miR-494 acts as a tumor suppressor in cervical cancer by inhibiting cell proliferation and invasion.
  • The tumor-suppressive function of miR-494 is mediated through the upregulation of its direct target, SOCS6.
  • Reduced miR-494 expression contributes to cervical cancer progression and may serve as a potential therapeutic target.

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