Related Experiment Video
Updated: Oct 1, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
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.
Background:
The oncogenic drivers of triple-negative breast cancer (TNBC), which is characterized by worst prognosis compared with other subtypes, are poorly understood. Although next-generation sequencing technology has facilitated identifying potential targets, few of the findings have been translated into daily clinical practice. The present study is aimed to explore ZNF703 (Zinc finger 703) function and its underlying mechanism in TNBC.
Methods:
ZNF703 expressions in tissue microarray were retrospectively examined by immunohistochemistry. The cell proliferation by SRB assay and colony formation assay, as well as cell cycle distribution by flow cytometry were assessed. The protein levels associated with possible underlying molecular mechanisms were evaluated by western blotting. Kaplan-Meier analysis was used to plot survival analysis.
Results:
Our data suggest that ZNF703 expressed in 34.2% of triple-negative human breast tumors by immunohistochemistry. In vitro, ZNF703 knockdown had potent inhibitory effects on TNBC cell proliferation and cell cycle, with cyclin D1, CDK4, CDK6, and E2F1 downregulated, while Rb1 upregulated. Moreover, Kaplan-Meier analysis showed that high mRNA expression of ZNF703 was correlated to worse overall survival (HR for high expression was 3.04; 95% CI, 1.22 to 7.57, P = 0.017).
Conclusions:
Taken together, the results identified that targeting ZNF703 contributed to the anti-proliferative effects in TNBC cells, due to induced G1-phase arrest. This study is the first to identify ZNF703 as a potentially important protein that is involved in TNBC progression.
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.
Related Concept Videos
Negative Regulator Molecules
Mitogens and the Cell Cycle
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Abnormal Proliferation
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

