Abstract
BackgroundRho GTPase-activating protein 10 (ARHGAP10), which catalyzes the conversion of active Rho GTPase to the inactive form, is downregulated in some cancers. However, little is known about ARHGAP10 in breast cancer.MethodsThe transcriptional expression level of ARHGAP10 in breast cancer was analyzed with the data downloaded from The Cancer Genome Atlas (TCGA) and Oncomine, then verified by reverse-transcription quantitative polymerase chain reaction (RT-qPCR) in 30 pairs of breast cancer tissues and the corresponding adjacent normal tissues. ARHGAP10 protein expression was examined by immunohistochemistry (IHC) in 190 breast cancer and 30 corresponding adjacent normal breast tissue samples. The associations between ARHGAP10 expression and clinicopathological characteristics of patients were analyzed, and Kaplan–Meier Plotter was used to assess the relationship between ARHGAP10 and relapse-free survival (RFS). Different expression levels of ARHGAP10 in response to chemotherapy agents were determined by GEO2R online tool. The potential biological functions of ARHGAP10 were analyzed by Gene Set Enrichment Analysis (GSEA) using data downloaded from TCGA.ResultsARHGAP10 mRNA and protein expression was lower in breast cancer tissues than in adjacent normal tissues. Low expression of ARHGAP10 was associated with advanced clinical TNM (cTNM) stage (pb = 0.001) and high Ki-67 index (p = 0.015). Low expression of ARHGAP10 indicated worse RFS (p = 0.0015) and a poor response to chemotherapy (p = 0.006). GSEA results showed that ARHGAP10 was involved in signaling pathways including protein export, nucleotide excision repair, base excision repair, focal adhesion, JAK-STAT pathway and the actin cytoskeleton.
Highlights
Breast cancer is the most prevalent malignant disease with highest incidence in females worldwide, accounting for 25% of all cancer cases and 15% of all cancer-related deaths among women according to the updated global cancer statistics (Chen et al, 2016)
The expression of ARHGAP10 was analyzed using data downloaded from The Cancer Genome Atlas (TCGA) and Curtis Breast in Oncomine (Curtis et al, 2012)
The results showed that ARHGAP10 was downregulated according to TCGA (p < 0.001) (Fig. 1A) and Curtis Breast of Oncomine (p < 0.001) (Fig. 1B)
Summary
Breast cancer is the most prevalent malignant disease with highest incidence in females worldwide, accounting for 25% of all cancer cases and 15% of all cancer-related deaths among women according to the updated global cancer statistics (Chen et al, 2016). Downregulated expression of ARHGAP10 correlates with advanced stage and high Ki-67 index in breast cancer. The management of breast cancer remains unsatisfactory, and the responses to treatment and patient outcomes vary among individuals partly because of the heterogeneity of tumors (Song et al, 2016). The transcriptional expression level of ARHGAP10 in breast cancer was analyzed with the data downloaded from The Cancer Genome Atlas (TCGA) and Oncomine, verified by reverse-transcription quantitative polymerase chain reaction (RT-qPCR) in 30 pairs of breast cancer tissues and the corresponding adjacent normal tissues. ARHGAP10 protein expression was examined by immunohistochemistry (IHC) in 190 breast cancer and 30 corresponding adjacent normal breast tissue samples. ARHGAP10 mRNA and protein expression was lower in breast cancer tissues than in adjacent normal tissues. Low expression of ARHGAP10 was associated with advanced clinical TNM (cTNM) stage (pb = 0.001) and high Ki-67 index (p = 0.015). GSEA results showed that ARHGAP10 was involved in signaling pathways including protein export, nucleotide excision repair, base excision repair, focal adhesion, JAK-STAT pathway and the actin cytoskeleton
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
