POC1A promotes malignant phenotypes in non-triple-negative breast cancer cell models with EMT- and Wnt/β-catenin-related alterations - Report - MDSpire
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POC1A promotes malignant phenotypes in non-triple-negative breast cancer cell models with EMT- and Wnt/β-catenin-related alterations
POC1A Enhances Malignant Characteristics in Non-Triple-Negative Breast Cancer
Overview
This study identifies POC1A as significantly upregulated in breast cancer, correlating with larger tumor size and advanced clinical stage.
Background
Breast cancer remains a leading cause of cancer-related morbidity and mortality among women globally. Identifying molecular markers associated with breast cancer progression is crucial.
Data Highlights
Dataset
AUC
TCGA cohort
0.879
GSE22820 cohort
0.901
Key Findings
POC1A is significantly upregulated in breast cancer tissues.
High POC1A expression correlates with larger tumor size and advanced clinical stage.
Multivariate Cox regression identifies high POC1A as an independent risk factor for poor prognosis (HR = 1.049, P = 0.014).
Kaplan–Meier analysis shows high POC1A mRNA expression is linked to poorer survival outcomes.
POC1A knockdown reduces cell proliferation, migration, and invasion in breast cancer cell lines.
Modulation of POC1A affects Wnt/β-catenin signaling and EMT-related markers.
Clinical Implications
The findings suggest that POC1A may serve as a potential biomarker for breast cancer prognosis. Understanding its role in malignant phenotypes could inform future therapeutic strategies targeting POC1A and related pathways.
Conclusion
POC1A is overexpressed in breast cancer and may contribute to aggressive tumor characteristics through modulation of key signaling pathways. Further validation of its clinical significance is necessary.
