GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling pathway

Mol Med Rep. 2021 Apr;23(4):246. doi: 10.3892/mmr.2021.11885. Epub 2021 Feb 4.

Abstract

Globally, thyroid cancer (TC) is considered to be the commonest endocrine malignancy. GINS complex subunit 2 (GINS2) belongs to the GINS complex family and is associated with cellular migration, invasion and growth. The present study aimed to investigate the underlying mechanisms of GINS2 on cell viability, migration and invasion in TC cells. By using MTT, wound healing and Transwell assays, the cell viability, migration and invasion were determined. Apoptosis was examined by immunofluorescence. Western blotting was used to detect protein expression levels. In the present study, biological function analysis demonstrated that GINS2 interference attenuated cell viability, migration and invasion in TC cell lines (K1 and SW579). It was discovered that, compared with the control group, GINS2 silencing induced apoptosis in TC cells. Additionally, GINS2 interference inhibited key proteins in the MAPK signaling pathway, including JNK, ERK and p38. According to these comparative experiments, GINS2 was considered to act a pivotal part in cell viability, migration and invasion of TC by regulating the MAPK signaling pathway and might be a potential therapeutic target for treating TC.

Keywords: GINS complex subunit 2; thyroid cancer; cell viability; migration and invasion; MAPK signaling pathway.

MeSH terms

  • Apoptosis*
  • Cell Line, Tumor
  • Cell Movement*
  • Cell Proliferation*
  • Chromosomal Proteins, Non-Histone / genetics
  • Chromosomal Proteins, Non-Histone / metabolism*
  • Humans
  • MAP Kinase Signaling System*
  • Neoplasm Invasiveness
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • Thyroid Neoplasms / genetics
  • Thyroid Neoplasms / metabolism*
  • Thyroid Neoplasms / pathology

Substances

  • Chromosomal Proteins, Non-Histone
  • GINS2 protein, human
  • Neoplasm Proteins

Grants and funding

The present study was supported by grants from National Natural Science Foundation of China (grant nos. 81873178 and 81904044), Shanghai Municipal Commission of Health and Family Planning (grant no. 201740084), Science and Technology Development Fund of Shanghai Pudong New Area (grant no. PKJ2019-Y15), Key Specialty Construction Project of Pudong Health and Family Planning Commission of Shanghai (grant no. PWZzk2017-21), Shanghai Pudong Commission of Health and Family Planning (grant no. PW2017B-11) and Talents Training Program of Seventh People's Hospital of Shanghai University of TCM (grant nos. XX2017-06 and XX2019-01).