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MicroRNA-618 modulates cell growth via targeting PI3K/Akt pathway in human thyroid carcinomas

L Yi1, Y Yuan1

  • 1Department of General Surgery, Suzhou Kowloon Hospital Shanghai Jiao Tong University, School of Medicine, Suzhou, Jiangsu 215021, P.R. China.

Indian Journal of Cancer
|July 26, 2016
PubMed
Abstract

Insights

MicroRNA-618 (miR-618) is downregulated in thyroid cancer (TC) and suppresses tumor growth by inhibiting the PI3K/Akt pathway. Restoring miR-618 may offer a therapeutic strategy for TC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are crucial regulators of gene expression implicated in various cancers.
  • Thyroid cancer (TC) is a significant health concern, and understanding its molecular underpinnings is vital for developing effective therapies.

Purpose of the Study:

  • To investigate the expression, function, and underlying mechanisms of microRNA-618 (miR-618) in human thyroid cancer (TC) cells.
  • To evaluate the potential of miR-618 as a therapeutic target in TC.

Main Methods:

  • Quantitative real-time PCR to assess miR-618 expression in TC tissues and adjacent normal tissues.
  • Cell proliferation assays (MTT) and cell cycle analysis (PI staining, flow cytometry) in TC cell lines with miR-618 overexpression.
  • Western blotting to analyze the impact of miR-618 on the PI3K/Akt signaling pathway.

Main Results:

  • miR-618 was confirmed to be downregulated in TC tissues.
  • Forced expression of miR-618 inhibited TC cell proliferation and induced G2/M cell cycle arrest.
  • miR-618 overexpression significantly suppressed the PI3K/Akt signaling pathway.
  • Re-expression of Akt reversed the growth-inhibitory effects of miR-618.

Conclusions:

  • miR-618 exhibits a growth-suppressive role in TC cells.
  • This suppressive effect is partially mediated through the targeting of the PI3K/Akt signaling pathway.
  • miR-618 represents a potential therapeutic agent for thyroid cancer.

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