ZMIZ2/MCM3 Axis Participates in Triple-Negative Breast Cancer Progression

Xiaopan Zou1,2, Meiyang Sun3, Xin Jiang1

  • 1Breast and Thyroid Surgery, Jilin Province People's Hospital, Changchun, 130021, China.

Oncology Research
|January 8, 2026
PubMed
Abstract

Insights

Zinc finger miz-type containing 2 (ZMIZ2) promotes triple-negative breast cancer (TNBC) progression by upregulating minichromosome maintenance complex component 3 (MCM3). This ZMIZ2/MCM3 axis involves key signaling pathways, offering potential therapeutic targets for aggressive TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies.
  • Understanding novel molecular mechanisms driving TNBC progression is critical.

Purpose of the Study:

  • To investigate the functional roles of zinc finger miz-type containing 2 (ZMIZ2) and minichromosome maintenance complex component 3 (MCM3) in TNBC.
  • To elucidate the regulatory relationship between ZMIZ2 and MCM3 and their downstream signaling pathways in TNBC.

Main Methods:

  • Correlation analysis of ZMIZ2 expression with TNBC clinical characteristics.
  • In vitro and in vivo experiments to assess ZMIZ2 and MCM3 functions in TNBC cells.
  • Transcriptome sequencing and pathway enrichment analysis (e.g., MAPK, mTOR, Wnt, Ras) using TCGA data.

Main Results:

  • High ZMIZ2 expression correlates with TNBC malignancy.
  • ZMIZ2 overexpression enhances TNBC proliferation, migration, invasion, and cell cycle progression while inhibiting apoptosis.
  • ZMIZ2 directly upregulates MCM3, which mediates ZMIZ2's oncogenic effects; high MCM3 expression indicates poor prognosis.

Conclusions:

  • ZMIZ2 and MCM3 are highly expressed and promote TNBC development.
  • The ZMIZ2/MCM3 axis, potentially involving Ras/MAPK, PI3K/AKT/mTOR, and Wnt pathways, drives TNBC progression.
  • Targeting the ZMIZ2/MCM3 axis may offer a novel therapeutic strategy for TNBC.

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