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Published on: September 13, 2018
Attenuated expression of SNF5 facilitates progression of bladder cancer via STAT3 activation
Hua Ding1, Yaqin Huang2, Jiazhong Shi2
1Department of Urology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Background:
SWI/SNF, a well-known ATP-dependent chromatin-remodeling complex, plays an essential role in several biological processes. SNF5, the core subunit of the SWI/SNF remodeling complex, inactivated in 95% of malignant rhabdoid tumors (MRT), highlighting its significance in tumorigenesis. However, the role of SNF5 in bladder cancer (BC) remains unknown. In this study, we aimed to investigate the function and potential clinical applicability of SNF5 in BC.
Methods:
Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) and Cancer Cell Line Encyclopedia (CCLE) databases were used to evaluate the clinical significance of SNF5 in BC. We performed Gene Set Enrichment Analysis (GSEA) and functional assays to investigate the role of SNF5 in BC. Genomics of Drug Sensitivity in Cancer (GDSC) and drug-susceptibility tests were performed to identify the potential value of SNF5 in the treatment of BC.
Results:
Low SNF5 expression conferred a poor prognosis and was significantly associated with the N-stage in BC. ROC curves indicated that SNF5 could distinguish BC from the normal tissues. In vitro and in vivo functional assays demonstrated that attenuated SNF5 expression could promote cell proliferation and enhance migration by STAT3 activation. We imputed that low SNF5 expression could confer greater resistance against conventional first-line drugs, including cisplatin and gemcitabine in BC. GDSC and drug-resistance assays suggested that low SNF5 expression renders T24 and 5637 cells high sensitivity to EGFR inhibitor gefitinib, and combination of EZH2 inhibitor GSK126 and cisplatin.
Conclusions:
To the best of our knowledge, the present study, for the first time, showed that low SNF5 expression could promote cell proliferation and migration by activating STAT3 and confer poor prognosis in BC. Importantly, SNF5 expression may be a promising candidate for identifying BC patients who could benefit from EGFR-targeted chemotherapy or cisplatin in combination with EZH2 inhibitor treatment regimens.
Insights
Low SNF5 expression in bladder cancer (BC) promotes tumor growth and migration via STAT3 activation, leading to poor prognosis. This finding suggests SNF5 as a potential biomarker for targeted therapies, including EGFR inhibitors.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genomics
Background:
- SWI/SNF chromatin-remodeling complex is crucial in biological processes.
- SNF5, a core SWI/SNF subunit, is frequently inactivated in malignant rhabdoid tumors (MRT).
- The role of SNF5 in bladder cancer (BC) pathogenesis and clinical significance is currently unknown.
Purpose of the Study:
- To investigate the function of SNF5 in bladder cancer (BC).
- To evaluate the potential clinical applicability and prognostic value of SNF5 in BC.
- To identify potential therapeutic strategies targeting SNF5 in BC.
Main Methods:
- Utilized data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Cancer Cell Line Encyclopedia (CCLE) databases.
- Performed Gene Set Enrichment Analysis (GSEA) and in vitro/in vivo functional assays.
- Conducted Genomics of Drug Sensitivity in Cancer (GDSC) and drug-susceptibility tests.
Main Results:
- Low SNF5 expression is associated with poor prognosis and advanced N-stage in BC.
- Attenuated SNF5 expression promotes BC cell proliferation and migration through STAT3 activation.
- Low SNF5 expression predicts resistance to cisplatin and gemcitabine, but sensitivity to EGFR inhibitor gefitinib and combination therapies (cisplatin + EZH2 inhibitor GSK126).
Conclusions:
- Low SNF5 expression promotes BC cell proliferation and migration by activating STAT3, correlating with poor prognosis.
- SNF5 serves as a potential biomarker for identifying BC patients who may benefit from EGFR-targeted therapy or combined cisplatin and EZH2 inhibitor treatment.
- This study provides novel insights into SNF5's role in BC and its therapeutic implications.
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