Retracted: Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR‐98/STAT3/Wnt/β‐catenin pathway axis

Abstract

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/β-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/β-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/β-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/β-catenin pathway axis. The SNHG16/miR-98/STAT3/Wnt/β-catenin pathway axis may provide a new strategy for bladder cancer treatment.

Prognostic and Predictive Values of the Autophagy Signature in Colon Cancer

“…lncRNA SNHG16 was showed to be regulated by the wnt pathway in colorectal cancer [40]. Additionally, SNHG16 has also been reported to associate with many other cancers, such as bladder cancer and pediatric neuroblastoma [41,42]. As of now, the remaining lncRNAs (AP006621.2, AL354993.2, AC048344.4, GS1-124K5.4, AC010973, AL590483.1, AL137782.1, STAG3L5P-PVRIG2P-PILRB, and AP001554.1) are rarely reported in the previous studies.…”

“…lncRNAs dominate the upstream portion of the RNA network and function as primary effectors of mRNAs, and several lncRNAs are identi ed as potential prognostic factors in COAD [20,30]. Among these 14 lncRNAs in the model, PCAT6, CASC9, MIR4435-2HG, SNHG16, and LINC00513 have been reported to play a role in the pathogenesis and prognosis of various cancer types (31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43). For example, CASC9 has been reported to be upregulated and conferred an oncogenic function in human hepatocellular carcinoma, oral carcinoma, gastric cancer, colorectal cancer, and esophageal cancer [28,[31][32][33].…”

<p><em>SNHG16</em>: A Novel Long-Non Coding RNA in Human Cancers</p>

“…They further stated that SNHG16 could sponge miR-98 and target STAT3 through the Wnt/ β-catenin pathway to act as an oncogene in bladder cancer. 55 And SNHG16 acts as a ceRNA in colorectal cancer cells to suppress miR-200a-3p and increase the expression of ZEB1 and, thereby, promote the expression of EMT-related genes, such as cadherins and vimentin, and promote cell migration and invasion. Similarly, Zhu et al revealed that silencing SNHG16 inhibits cell migration and invasion, and EMT in vitro, indicating that SNHG16 is involved in the tumorigenesis of cervical cancer (CC).…”

Long non‐coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR‐205 and modulating Smad2

“…to date, the lncRNA small nucleolar RNA host gene 16 (SNHG16) has been well-documented in several types of cancers including bladder cancer, liver cancer, cervical cancer, glioma and osteosarcoma. [15][16][17][18] However, the role of SNHG16 in CVDs has not been explored yet.…”

“…The lncRNA myosin heavy‐chain‐associated RNA transcripts were found to protect the heart from pathological hypertrophy . Up to date, the lncRNA small nucleolar RNA host gene 16 (SNHG16) has been well‐documented in several types of cancers including bladder cancer, liver cancer, cervical cancer, glioma and osteosarcoma . However, the role of SNHG16 in CVDs has not been explored yet.…”