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Updated: Dec 19, 2025

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
LncRNA BRE-AS1 acts as a tumor suppressor factor in bladder cancer via mediating STAT3
1Department of Urology, Jingmen No. 2 People's Hospital, Jingmen, China. Lijianxin19790819@icloud.com.
Objective:
Long non-coding RNA (lncRNA) has been verified to regulate several cancers, including bladder cancer (BC). Our study aimed to elucidate the expression, function, and mechanism of lncRNA BRE-AS1 in BC.
Patients And Methods:
Relative expression of lncRNA BRE-AS1 in 77 BC tissues and adjacent normal tissues was determined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Expression of lncRNA BRE-AS1 in T24 and EJ cells was up-regulated using lentivirus transfection. Cell counting kit-8 (CCK-8) assay and colony formation assay were used to assess the proliferation of T24 and EJ cells influenced by lncRNA BRE-AS1. Also, the influence of lncRNA BRE-AS1 on cell apoptosis and cell cycle was measured using flow cytometry. Western blot was employed to explore the downstream molecules for lncRNA BRE-AS1 in BC. In vivo, xenograft formation experiment was established in nude mice to study the function of lncRNA BRE-AS1 in BC.
Results:
LncRNA BRE-AS1 showed significantly decreased expression in BC tissues than the paired normal tissues. In vitro experiments demonstrated that over-expression of lncRNA BRE-AS1 inhibited cell proliferation but promoted cell apoptosis of EJ and T24 cells. STAT3 was determined as a target for lncRNA BRE-AS1. In vivo, up-regulation of lncRNA BRE-AS1 reduced cancer growth in nude mice bearing BC via repressing the phosphorylation of STAT3.
Conclusions:
LncRNA BRE-AS1 was down-regulated in BC tissues. Over-expression of lncRNA BRE-AS1 inhibited BC cell proliferation in vitro and in vivo via repressing the phosphorylation of STAT3. This might provide a new sight for the understanding of BC progression and biotherapy.
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