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LncRNA XIST/miR-34a axis modulates the cell proliferation and tumor growth of thyroid cancer through MET-PI3K-AKT

Hua Liu1, Haoyu Deng1, Yajie Zhao1

  • 1Nuclear Medicine Department, Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.

Journal of Experimental & Clinical Cancer Research : CR
|November 23, 2018
PubMed
Abstract

Insights

Long non-coding RNA XIST is upregulated in thyroid cancer, promoting tumor growth by sponging miR-34a. This interaction impacts the MET-PI3K-AKT pathway, offering a novel target for thyroid cancer therapy.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Thyroid cancer is a prevalent endocrine malignancy.
  • Understanding its molecular mechanisms is crucial for effective diagnosis and treatment.
  • lncRNA-miRNA-mRNA interactions offer a novel therapeutic avenue.

Purpose of the Study:

  • Investigate the role of XIST (X-inactive specific transcript) in thyroid cancer.
  • Elucidate the interaction between XIST, miR-34a, and MET signaling.
  • Provide a basis for targeted thyroid cancer therapy.

Main Methods:

  • Determined XIST expression and function in thyroid cancer.
  • Screened for miRNA targets of XIST, identifying miR-34a.
  • Evaluated XIST-miR-34a binding and their effect on the MET-PI3K-AKT pathway.

Main Results:

  • XIST was upregulated in thyroid cancer tissues and cell lines.
  • XIST knockdown inhibited cell proliferation and tumor growth.
  • XIST sponged miR-34a, leading to MET upregulation and PI3K/AKT phosphorylation.
  • MET positively correlated with XIST and negatively with miR-34a in tissues.

Conclusions:

  • XIST acts as a competing endogenous RNA (ceRNA) for miR-34a in thyroid cancer.
  • This interaction modulates the MET-PI3K-AKT pathway, affecting tumor growth.
  • Findings support XIST as a potential therapeutic target for thyroid cancer.
Keywords:
METPI3K/AKTThyroid cancerXISTmiR-34a

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