ZNF703 promotes triple-negative breast cancer cells through cell-cycle signaling and associated with poor prognosis

Xi Zhang1,2, Xin Mu3, Ou Huang4

  • 1Department of Breast Oncology, The First Hospital of Quanzhou Affiliated to Fujian Medical University, Anji Rd, 362000, Quanzhou, China. Hee_rainday@foxmail.com.

BMC Cancer
|March 3, 2022
PubMed
Abstract

Insights

This study reveals Zinc finger 703 (ZNF703) is highly expressed in triple-negative breast cancer (TNBC) and targeting it inhibits cancer cell proliferation. High ZNF703 expression correlates with poorer survival in TNBC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Triple-negative breast cancer (TNBC) has a poor prognosis, and its drivers are not well understood.
  • Identifying actionable targets for TNBC remains a clinical challenge.
  • This research investigates the role of Zinc finger 703 (ZNF703) in TNBC.

Purpose of the Study:

  • To explore the function of ZNF703 in triple-negative breast cancer.
  • To elucidate the underlying molecular mechanisms of ZNF703 in TNBC progression.

Main Methods:

  • Immunohistochemistry was used to examine ZNF703 expression in human breast tumors.
  • In vitro assays (SRB, colony formation, flow cytometry) assessed cell proliferation and cell cycle.
  • Western blotting evaluated protein levels, and Kaplan-Meier analysis assessed survival data.

Main Results:

  • ZNF703 was expressed in 34.2% of TNBC tissues.
  • ZNF703 knockdown inhibited TNBC cell proliferation and induced G1-phase arrest.
  • High ZNF703 mRNA levels correlated with significantly worse overall survival in TNBC patients.

Conclusions:

  • Targeting ZNF703 demonstrates anti-proliferative effects in TNBC cells by inducing G1-phase arrest.
  • ZNF703 is identified as a potential therapeutic target and prognostic biomarker for TNBC.
  • This study provides novel insights into ZNF703's role in TNBC pathogenesis.

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