标题：Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR-98/STAT3/Wnt/-catenin pathway axis
作者：Feng, Feng; Chen, Aiping; Huang, Junjian; Xia, Qinghua; Chen, Yougen; Jin, Xunbo
作者机构：[Feng, Feng; Xia, Qinghua; Chen, Yougen; Jin, Xunbo] Shandong Univ, Shandong Prov Hosp, Dept Minimally Invas Urol, 324 Jing Wu Rd, Jinan 250021, Shand 更多
通讯作者地址：[Feng, F]Shandong Univ, Shandong Prov Hosp, Dept Minimally Invas Urol, 324 Jing Wu Rd, Jinan 250021, Shandong, Peoples R China.
来源：JOURNAL OF CELLULAR BIOCHEMISTRY
关键词：bladder cancer; long noncoding RNA (lncRNA); miR-98; small nucleolar RNA; host gene 16 (SNHG16); signal transducer and activator of transcription; 3 (STAT3); Wnt; -catenin pathway
摘要：This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detected. T24 cells were then transfected with sh-SNHG16 to further investigate the effects of suppression of SNHG16 on T24 cell proliferation, apoptosis, migration, and invasion. In addition, the regulatory relationships between SNHG16 and miR-98 as well as the target of miR-98 were explored. Besides, the association between SNHG16 and the Wnt/-catenin pathway was further elucidated. The SNHG16 expression was upregulated in the tumor tissues and plasma of patients with bladder cancer, as well as bladder cancer cells. Suppression of SNHG16 inhibited T24 cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro. In addition, SNHG16 negatively regulated miR-98 expression and regulated the malignant behaviors of T24 cells through sponging miR-98. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a functional target of miR-98, and miR-98 regulated the malignant behaviors of bladder cancer cells by targeting STAT3. Besides, suppression of SNHG16 inhibited the activation of the Wnt/-catenin pathway, which was further regulated by miR-98 and STAT3, indicating that the effects of SNHG16/miR-98/STAT3 on T24 cells were achieved through the Wnt/-catenin pathway. Our findings reveal that long noncoding RNAs SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR-98/STAT3/Wnt/-catenin pathway axis. The SNHG16/miR-98/STAT3/Wnt/-catenin pathway axis may provide a new strategy for bladder cancer treatment.