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ZNF292 suppresses proliferation of ESCC cells through ZNF292/SKP2/P27 signaling axis

Wei Gong1, Jiancheng Xu1, Guangchao Wang1

  • 1State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.

Chinese Journal of Cancer Research = Chung-Kuo Yen Cheng Yen Chiu
|February 7, 2022
PubMed
Abstract

Insights

Zinc finger protein 292 (ZNF292) acts as a tumor suppressor in esophageal squamous cell carcinoma (ESCC). Its knockdown promotes cancer cell growth by activating SKP2/P27 signaling, leading to G1/S cell cycle progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Zinc finger protein 292 (ZNF292) is increasingly recognized for its tumor-suppressive functions across various cancers.
  • The specific role and underlying mechanisms of ZNF292 in esophageal squamous cell carcinoma (ESCC) remain largely unexplored.

Purpose of the Study:

  • To investigate the functional role of ZNF292 in the prognosis and progression of ESCC.
  • To elucidate the molecular mechanisms by which ZNF292 influences ESCC cell growth and cell cycle regulation.

Main Methods:

  • Bioinformatic analysis and immunohistochemistry (IHC) were employed to assess ZNF292 expression and its correlation with ESCC prognosis.
  • Cellular assays including proliferation, colony formation, and flow cytometry were conducted to evaluate the impact of ZNF292 depletion on ESCC cell growth and cell cycle.
  • Quantitative real-time PCR (qRT-PCR), Western blot, and chromatin immunoprecipitation (ChIP) assays were utilized to determine the molecular interactions and regulatory pathways involved.

Main Results:

  • Low ZNF292 expression was significantly associated with poor prognosis in ESCC patients.
  • ZNF292 was found to be downregulated in ESCC tumor tissues compared to adjacent and normal tissues.
  • ZNF292 depletion enhanced ESCC cell proliferation and promoted G1/S phase transition, mediated by increased SKP2 expression and subsequent P27 degradation.

Conclusions:

  • ZNF292 functions as a tumor suppressor in ESCC by inhibiting cell proliferation and G1/S cell cycle progression.
  • ZNF292 knockdown facilitates G1/S cell cycle transition through transcriptional activation of SKP2, leading to enhanced P27 ubiquitin-degradation.
  • These findings highlight the ZNF292/SKP2/P27 axis as a potential therapeutic target in ESCC.
Keywords:
ESCCSKP2ZNF292cell cycle

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