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 ... -  《-》

Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.

Long noncoding RNA paternally expressed gene 10 (lncRNA PEG10) has been certified to regulate cell proliferation, metastasis, and apoptosis in diversified cancer cells. Nevertheless, the functions of PEG10 in bladder cancer cells remain uninvestigated. We tried to probe the impacts of PEG10 on proliferation, migration, and invasion of bladder cancer cells. PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/β-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/β-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-29b-Wnt/β-catenin-JNK axis.

Liang T ，Wang Y ，Wang Y ，Wang Y ... -  《-》

LncRNA SNHG16 promotes proliferation and migration in laryngeal squamous cell carcinoma via the miR-140-5p/NFAT5/Wnt/β-catenin pathway axis.

Wan L ，Gu D ，Li P 《-》

Long non-coding RNA SNHG20 promotes bladder cancer via activating the Wnt/β-catenin signalling pathway.

Zhao Q ，Gao S ，Du Q ，Liu Y ... -  《-》

Investigations on the mechanism of progesterone in inhibiting endometrial cancer cell cycle and viability via regulation of long noncoding RNA NEAT1/microRNA-146b-5p mediated Wnt/β-catenin signaling.

Progesterone is often used to protect the endometrium and prevent endometrial cancer. An intensive study on its molecular mechanism in endometrial cancer would contribute to the development of more promising therapies. Relevant lncRNAs and mRNAs expression data in endometrial cancer cell line Ishikawa pretreated and post-treated with progesterone were derived from Gene Expression Omnibus (accession no. GSE29435), and then we analyzed long noncoding RNAs and mRNAs with differential expressions in two different conditions. The Cytoscape software, TargetScan, miRanda, and Human microRNA Disease Database (HMDD) websites were employed. Gene set enrichment analysis (GSEA) was used to determine related Kyoto Encyclopedia of Genes and Genomes pathways alteration in Ishikawa cells treated with progesterone. In addition to bioinformatics analysis, Reverse Transcription-Polymerase Chain Reaction (RT-PCR), Western blot, and dual-luciferase reporter assays were performed. The impact of progesterone on cell propagation and cell cycle was testified by colony formation and flow cytometry analysis. LncRNA nuclear enriched abundant transcript 1 (NEAT1) was the most significantly downregulated lncRNA in endometrial cancer cells treated with progesterone. Lymphoid enhancing factor 1 (LEF1) was positively associated with NEAT1, and eventually hsa_miR-146b-5p was validated to target both LEF1 and NEAT1. Wnt/β-catenin signaling pathway was identified to involve in endometrial cancer. NEAT1 or LEF1 was overexpressed in endometrial cancer cells while downregulated following post-treatment with progesterone. Conversely, miR-146b-5p was notably decreased in Ishikawa cells while upregulated after treatment with progesterone. Downstream gene c-myc or MMP9 regulated by upstream gene LEF1 in Wnt/β-catenin signaling pathway was remarkably increased in Ishikawa cells and positively related with NEAT1. Progesterone inhibited cell cycle and viability through regulating NEAT1/miR-146b-5p axis via Wnt/β-catenin signaling pathway. Progesterone exerted suppressive influence on endometrial cancer progression via regulation of lncRNA NEAT1/miR-146b-5p-mediated Wnt/β-catenin signaling pathway, which might reveal new strategies for developing more effective therapeutics. © 2018 IUBMB Life, 71(1):223-234, 2019.

Huang X ，Zhong R ，He X ，Deng Q ，Peng X ，Li J ，Luo X ... -  《-》