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GSG2 promotes thyroid cancer via stabilizing AURKB and activating AKT pathway

Fenghua Zhang1, Chiming Huang2

  • 1Department of Thyroid and Breast Surgery, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.

Aging
|March 5, 2024
PubMed

Insights

The gene GSG2 is upregulated in thyroid cancer and promotes tumor growth by stabilizing AURKB and activating the AKT pathway. Inhibiting GSG2 may offer a new therapeutic strategy for thyroid cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Thyroid cancer is the most common endocrine cancer globally, with increasing incidence.
  • The role of GSG2 (also known as KIAA0101) in thyroid cancer development is largely unknown.
  • Previous research suggests GSG2 involvement in other cancers.

Purpose of the Study:

  • To investigate the functional significance of GSG2 in human thyroid cancer.
  • To elucidate the molecular mechanisms underlying GSG2's role in thyroid carcinogenesis.
  • To explore GSG2 as a potential therapeutic target.

Main Methods:

  • Analysis of GSG2 expression in thyroid cancer tissues and cell lines.
  • GSG2 depletion experiments in thyroid cancer cells.
  • Investigation of downstream targets, including AURKB and the AKT pathway.
  • Validation using gene overexpression and pathway activators.

Main Results:

  • GSG2 expression is significantly upregulated in thyroid cancer tissues and cell lines, correlating with pathological stage and prognosis.
  • GSG2 depletion suppresses thyroid cancer cell proliferation and tumor growth.
  • GSG2 stabilizes AURKB by inhibiting SMURF1-mediated ubiquitination.
  • GSG2 activates the AKT pathway, evidenced by increased p-AKT levels.

Conclusions:

  • GSG2 plays a critical role in thyroid cancer development and progression.
  • GSG2 regulates thyroid cancer via AURKB stabilization and AKT pathway activation.
  • GSG2 represents a promising therapeutic target for thyroid cancer treatment.
Keywords:
AKT pathwayAURKBGSG2cell phenotypesthyroid cancer

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