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UBE2C promotes cell cycle progression and suppresses DNA damage-induced apoptosis in triple-negative breast cancer

Qin Hu1, Kewu Wang2, Chuanrong Chen3

  • 1Anhui Medical University, Hefei, Anhui 230032, China; Department of Oncology, Wuhu Hospital, East China Normal University (The Second People's Hospital, Wuhu), Wuhu, Anhui 241000, China.

DNA Repair
|October 14, 2025
PubMed
Abstract

Insights

Ubiquitin-conjugating enzyme E2C (UBE2C) is overexpressed in triple-negative breast cancer (TNBC), promoting cell survival by regulating cell cycle, DNA repair, and apoptosis. UBE2C may serve as a therapeutic target for TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is aggressive and lacks targeted therapies.
  • Dysfunctional cell cycle, DNA repair, and apoptosis drive TNBC progression.
  • UBE2C, a mitotic regulator, is implicated in cancer but its role in TNBC is unclear.

Purpose of the Study:

  • Investigate UBE2C expression in TNBC.
  • Determine the functional role of UBE2C in TNBC development.

Main Methods:

  • Analyzed TCGA and GTEx transcriptomic data for UBE2C levels and clinical relevance.
  • Utilized Gene Set Enrichment Analysis (GSEA) to identify UBE2C-associated pathways.
  • Performed functional assays in MDA-MB-231 cells to assess UBE2C's impact on cell cycle, DNA damage, and apoptosis.

Main Results:

  • UBE2C was significantly overexpressed in TNBC tissues and cell lines (P < 0.01).
  • High UBE2C expression correlated with reduced overall survival (P = 0.01).
  • UBE2C overexpression accelerated cell cycle progression, reduced DNA damage, and suppressed apoptosis.

Conclusions:

  • UBE2C promotes TNBC cell survival via cell cycle, DNA repair, and apoptosis modulation.
  • UBE2C is a potential biomarker and therapeutic target for TNBC.
  • Combination therapy with DNA-damaging agents may be beneficial for TNBC patients.
Keywords:
ApoptosisCell cycleDNA damage repairTriple-negative breast cancerUBE2C

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