CCDC68 Upregulation by IL-6 Promotes Endometrial Carcinoma Progression

J Interferon Cytokine Res. 2021 Jan;41(1):12-19. doi: 10.1089/jir.2020.0193.

Abstract

The elevation of circulating interleukin 6 (IL-6) is one of the major molecular characteristics of endometrial carcinoma. In this study, we investigated the role of coiled-coil domain-containing 68 (CCDC68) in IL-6-associated endometrial carcinoma progression. CCDC68 expression levels and the activation of IL-6 pathway were detected by qPCR and Western blot. Stable CCDC68 knockdown Ishikawa and RL-95 cells were created to investigate cancer cell proliferation, migration, and invasion with or without IL-6 administration. Kaplan-Meier's analysis was used to determine the correlation between CCDC68 expression and overall survival or recurrence-free survival in endometrial carcinoma patients. CCDC68 expression level is significantly uregulated by IL-6 stimulation. Increased CCDC68 expression predicts poor prognosis in endometrial carcinoma patients. CCDC68 knockdown dramatically inhibit IL-6-associated cancer cell proliferation, migration, invasion, and downregulate the expression of proto-oncogenes in endometrial carcinoma cells. CCDC68 acts as a cancer-promoting factor in IL-6-stimulated endometrial carcinoma cells, and blocking the expression of CCDC68 might be a novel therapeutic strategy for the endometrial carcinoma treatment.

Keywords: CCDC68; IL-6; endometrial carcinoma; migration; proliferation.

MeSH terms

  • Endometrial Neoplasms / immunology*
  • Endometrial Neoplasms / pathology
  • Female
  • Humans
  • Interleukin-6 / immunology*
  • Tumor Cells, Cultured
  • Tumor Suppressor Proteins / immunology*
  • Up-Regulation / immunology*

Substances

  • CCDC68 protein, human
  • IL6 protein, human
  • Interleukin-6
  • Tumor Suppressor Proteins