Downregulated expression of ARHGAP10 correlates with advanced stage and high Ki-67 index in breast cancer

Yujing Li1, Beilei Zeng1, Yunhai Li1

  • 1Chongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Peerj
|August 10, 2019
PubMed
Abstract

Insights

Rho GTPase-activating protein 10 (ARHGAP10) is downregulated in breast cancer, correlating with advanced stage and poor relapse-free survival. Low ARHGAP10 expression indicates a worse response to chemotherapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Rho GTPase-activating protein 10 (ARHGAP10) regulates Rho GTPase activity and is implicated in various cancers.
  • Its role in breast cancer remains largely unexplored.

Purpose of the Study:

  • To investigate the expression levels of ARHGAP10 in breast cancer.
  • To analyze the association between ARHGAP10 expression and clinicopathological features, patient survival, and chemotherapy response.

Main Methods:

  • Analysis of ARHGAP10 mRNA expression using TCGA and Oncomine data.
  • Validation of ARHGAP10 mRNA and protein expression via RT-qPCR and immunohistochemistry in patient tissues.
  • Correlation analysis with clinicopathological characteristics and survival outcomes (Kaplan-Meier Plotter).
  • Assessment of chemotherapy response and pathway analysis (GSEA).

Main Results:

  • ARHGAP10 mRNA and protein levels were significantly lower in breast cancer tissues compared to normal adjacent tissues.
  • Low ARHGAP10 expression correlated with advanced clinical TNM stage and high Ki-67 index.
  • Reduced ARHGAP10 expression was associated with worse relapse-free survival and poorer response to chemotherapy.
  • GSEA identified ARHGAP10 involvement in pathways such as protein export, DNA repair, focal adhesion, JAK-STAT signaling, and actin cytoskeleton regulation.

Conclusions:

  • ARHGAP10 is downregulated in breast cancer and serves as a potential biomarker for disease progression and treatment response.
  • Its dysregulation impacts key cellular processes, highlighting its significance in breast cancer pathogenesis.

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