Journal
ONCOTARGET
Volume 6, Issue 11, Pages 9220-9239Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.3312
Keywords
EMP2; CREB1; urinary bladder urothelial carcinoma; tumor suppressor
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Funding
- Ministry of Science and Technology, Taiwan [103-2314-B-110-001]
- Ministry of Health and Welfare, Taiwan [MOHW104-TDU-B-212-124-003]
- High-throughput Genome Analysis Core Facility of National Core Facility Program for Biotechnology, Taiwan [102-2319-B-010-001]
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In this study, we report that EMP2 plays a tumor suppressor role by inducing G(2)/M cell cycle arrest, suppressing cell viability, proliferation, colony formation/anchorage-independent cell growth via regulation of G(2)/M checkpoints in distinct urinary bladder urothelial carcinoma (UBUC)-derived cell lines. Genistein treatment or exogenous expression of the cAMP responsive element binding protein 1 (CREB1) gene in different UBUC-derived cell lines induced EMP2 transcription and subsequent translation. Mutagenesis on either or both cAMP-responsive element(s) dramatically decreased the EMP2 promoter activity with, without genistein treatment or exogenous CREB1 expression, respectively. Significantly correlation between the EMP2 immunointensity and primary tumor, nodal status, histological grade, vascular invasion and mitotic activity was identified. Multivariate analysis further demonstrated that low EMP2 immunoexpression is an independent prognostic factor for poor disease-specific survival. Genistein treatments, knockdown of EMP2 gene and double knockdown of CREB1 and EMP2 genes significantly inhibited tumor growth and notably
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