Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway.

More and more studies have shown that long non-coding RNAs (lncRNAs) play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. LncRNA long intergenic noncoding RNA 00511 (linc00511) is one of the lncRNAs highly expressed in bladder cancer tissues and cells. However, little is known about the roles and mechanisms of linc00511 in bladder cancer. Here, we demonstrated that linc00511 was highly expressed in bladder cancer tissues and cells. Linc00511 knockdown could cause the cell proliferation suppression and cell cycle arrest, which were mediated by p18, p21, CDK4, cyclin D1 and phosphorylation Rb. Suppressed linc00511 could induce the apoptosis in T24 and BIU87 cells via activating the caspase pathway. Down-regulation of linc00511 could also suppress the migration and invasion of T24 and BIU87 cells. In addition, we found that the expression of linc00511 was negatively correlated with that of miR-15a-3p in the clinical bladder cancer samples. Further mechanistic studies showed that linc00511 knockdown induced proliferation inhibition, and apoptosis increase might be regulated through suppressing the activities of Wnt/β-catenin signaling pathway. Thus, we revealed that knockdown of linc00511 suppressed the proliferation and promoted apoptosis of bladder cancer cells through suppressing the activities of Wnt/β-catenin signaling pathway. Moreover, we suggested that linc00511 could be a potential therapeutic target and novel biomarker in bladder cancer.

Li J ，Li Y ，Meng F ，Fu L ，Kong C ... -  《-》

Knockdown of lncRNA SNHG7 inhibited cell proliferation and migration in bladder cancer through activating Wnt/β-catenin pathway.

It is identified that long non-coding RNAs (lncRNAs) play important roles in tumorigenesis. LncRNA SNHG7 has been found to be an oncogene in varieties of tumors including bladder cancer. However, its potential regulatory mechanism in bladder cancer still remains unknown. In this study, we discovered that the expression levels of SNHG7 were significantly increased in bladder cancer tissues and cell lines. Patients with high expression level of SNHG7 suffered from poor prognosis. Additionally, knockdown of SNHG7 induced declined cell viability, proliferation as well as G0/G1 cell cycle arrest. Furthermore, we found that cell migratory ability was markedly reduced after silencing SNHG7. Next, we verified that knockdown of SNHG7 reduced the protein level of β-catenin and thus decreased the level of its downstream targets including c-myc, cyclin D1 and E-cadherin, implying that SNHG7 might impact bladder cancer via Wnt/β-catenin pathway. Subsequently, the rescue assays performed in SNHG7 silenced T24 cells by using activator of Wnt/β-catenin signaling elucidated that re-activation of this pathway partly restored the inhibitory effects of SNHG7 suppression on biological behaviors of T24 cells. Collectively, SNHG7 elicited carcinogenic functions in bladder cancer partially via activating Wnt/β-catenin signaling pathway, suggesting a potential target for the treatment and prognosis of bladder cancer.

Chen Y ，Peng Y ，Xu Z ，Ge B ，Xiang X ，Zhang T ，Gao L ，Shi H ，Wang C ，Huang J ... -  《-》

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

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.

Feng F ，Chen A ，Huang J ，Xia Q ，Chen Y ，Jin X ... -  《-》

Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.

Zhao F ，Lin T ，He W ，Han J ，Zhu D ，Hu K ，Li W ，Zheng Z ，Huang J ，Xie W ... -  《Oncotarget》

The lncRNA LINC00675 regulates cell proliferation, migration, and invasion by affecting Wnt/β-catenin signaling in cervical cancer.

Cervical cancer is one of the most common gynecological malignancies worldwide. Recently, the long noncoding RNAs (lncRNAs) have been shown to play essential roles in cervical cancer development and progression. This study investigated the role of lncRNA LINC00675 in cervical cancer and explored the relevant molecular mechanisms. LINC00675 expression was determined by quantitative real-time polymerase chain reaction; cell proliferation, migration and invasion were determined by Cell Counting Kit-8, Transwell migration, and invasion assays, respectively; cell apoptosis was measured by flow cytometry; protein levels were measured by western blot assay. LINC00675 was upregulated in the cervical cancer tissues and cell lines, and upregulation of LINC00675 was positively correlated with advanced clinical stage and poor prognosis in patients with cervical cancer. Overexpression of LINC00675 promoted cervical cancer cell proliferation, invasion, and migration. In addition, overexpression of LINC00675 inhibited cell apoptosis, increased the protein level of Bcl-2, and decreased the protein level of Bax in cervical cancer cells. However, knockdown of LINC00675 played a contrasting role in cervical cancer cells. Overexpression of LINC00675 also increased the activity of Wnt/β-catenin signaling in cervical cancer cells, whereas knockdown of LINC00675 suppressed the activity of Wnt/β-catenin signaling. In addition, lithium chloride treatment attenuated the effects of LIC00675 knockdown on CaSki cell proliferation, invasion and migration. In vivo tumor growth study showed that knockdown of LINC00675 suppressed tumor growth, increased the protein levels of Bax and GSK-3β, and decreased the protein levels of Bcl-2 and β-catenin in isolated tumor tissues. In conclusion, our results implied that LINC00675 promoted cancer cell proliferation, migration, and invasion, and inhibit apoptosis likely by modulating the Wnt/β-catenin pathway.

Ma S ，Deng X ，Yang Y ，Zhang Q ，Zhou T ，Liu Z ... -  《-》