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Gene ; 710: 193-201, 2019 Aug 20.
Article in English | MEDLINE | ID: mdl-31176734

ABSTRACT

Accumulative researches have demonstrated the critical functions of long non-coding RNAs (lncRNAs) in the progression of malignant tumors, including bladder cancer (BC). Our previous studies showed that lnc-DILC was an important tumor suppressor gene in both liver cancer and colorectal cancer. However, the role of lnc-DILC in BC remains to be elucidated. In the present study, we for first found that lnc-DILC was downregulated in human bladder cancer tissues. Lnc-DILC overexpression suppressed the proliferation, metastasis and expansion of bladder cancer stem cells (CSCs). Mechanically, lnc-DILC suppressed BC cells progression via STAT3 pathway. Special STAT3 inhibitor S3I-201 diminished the discrepancy of growth, metastasis and self-renewal ability between lnc-DILC-overexpression BC cells and their control cells, which further confirmed that STAT3 was acquired for lnc-DILC-disrupted BC cell growth, metastasis and self-renewal. Taken together, our results suggest that lnc-DILC is a novel bladder tumor suppressor and indicate that lnc-DILC inhibits BC progression via inactivating STAT3 signaling.


Subject(s)
Down-Regulation , RNA, Long Noncoding/genetics , Signal Transduction , Urinary Bladder Neoplasms/genetics , Aminosalicylic Acids/pharmacology , Benzenesulfonates/pharmacology , Cell Line, Tumor , Cell Proliferation , Cell Self Renewal/drug effects , Disease Progression , Gene Expression Regulation, Neoplastic , Humans , Neoplasm Metastasis , Neoplastic Stem Cells/drug effects , Neoplastic Stem Cells/metabolism , STAT3 Transcription Factor/antagonists & inhibitors , STAT3 Transcription Factor/genetics , Signal Transduction/drug effects
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