Research Paper Volume 16, Issue 6 pp 5091—5107

GSG2 promotes thyroid cancer via stabilizing AURKB and activating AKT pathway

Fenghua Zhang1, , Chiming Huang2, ,

  • 1 Department of Thyroid and Breast Surgery, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China
  • 2 Thyroid Hernia Surgery, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Yuexiu, Guangzhou 510182, Guangdong Province, China

Received: March 28, 2023       Accepted: January 29, 2024       Published: March 4, 2024
How to Cite

Copyright: © 2024 Zhang and Huang. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Thyroid cancer stands out as the most prevalent endocrine cancer, with its incidence on a global rise. While numerous studies have delved into the roles of GSG2 in the progression of various malignancies, its involvement in thyroid cancer remains relatively unexplored. Therefore, this study was initiated to assess the functional importance of GSG2 in human thyroid cancer development. Our findings revealed a notable upregulation of GSG2 in both thyroid cancer tissues and cell lines, demonstrating a significant correlation with the pathological stage and patients’ prognosis. Depletion of GSG2 in thyroid cancer cells resulted in suppressed malignant cell development and inhibited tumor outgrowth. Crucially, our investigation identified AURKB as a downstream gene of GSG2. GSG2 exhibited its regulatory role by stabilizing AURKB, countering SMURF1-mediated ubiquitination of AURKB. Furthermore, overexpressing AURKB restored the functional consequences of GSG2 depletion in thyroid cancer cells. Additionally, we proposed the involvement of the AKT pathway in GSG2-mediated regulation of thyroid cancer. Intriguingly, the reversal of cell phenotype alterations in GSG2-depleted cells following an AKT activator underscored the potential link between GSG2 and the AKT pathway. At the molecular level, GSG2 knockdown downregulated p-AKT, an effect partially restored after AKT activator treatment. In summary, our study concluded that GSG2 played a pivotal role in thyroid carcinogenesis, underscoring its potential as a therapeutic target for thyroid cancer.


AURKB: Aurora kinase B; WDTCs: Well-differentiated thyroid cancers; PDTC: Poorly differentiated thyroid cancer; ATC: Anaplastic thyroid cancer; CPC: Chromosomal passenger complex; ccRCC: Clear cell renal cell carcinoma; EMT: Epithelial-mesenchymal transition; TMA: Thyroid cancer tissue microarray; ATCC: American type culture collection.