Long non-coding RNA CYTOR modulates cancer progression through miR-136-5p/MAT2B axis in renal cell carcinoma.

To explore the role of long noncoding RNAs (lncRNAs) cytoskeleton regulator RNA (CYTOR) in renal cell carcinoma (RCC). The levels of CYTOR in RCC tissues and cell lines were detected by RT-qPCR. 786-O and Caki-1 cells were transfected with CYTOR-shRNA or pcDNA-CYTOR respectively, or co-transfected with CYTOR-shRNA and miR-136-5p inhibitor, or co-transfected with miR-136-5p mimic and pcDNA-MAT2B. MTT assay, Transwell assay and flow cytometry were used to evaluate cell proliferation, invasion and apoptosis. The relationship between lncRNA CYTOR and miRNA-136-5p was detected by dual luciferase reporter gene and RNA pull down assays, and the targeted relationship between miRNA-136-5p and MAT2B was verified by dual luciferase reporter gene assay. The interaction between MAT2B and BAG3 protein was verified by co-IP experiment. The role of lncRNA CYTOR in vivo was also examined. LncRNA CYTOR was up-regulated in RCC tissues and cell lines, and miR-136-5p was down-regulated in renal carcinoma cell lines and tissues. Downregulation of CYTOR inhibited cell proliferation and invasion and promoted apoptosis. miR-136-5p was sponged by lncRNA CYTOR, which negatively regulated the development of RCC. MAT2B was a target gene of miR-136-5p. MAT2B protein interacted directly with BAG3 protein to affect the proliferation, invasion and apoptosis of RCC cells. In vivo experiments showed that the expression level of miR-136-5p was increased, and MAT2B expression was decreased after CYTOR knockdown, thereby inhibiting the development of RCC. LncRNA CYTOR promoted the progression of RCC by targeting miR-136-5p to regulate the target gene MAT2B, which interacted with BAG3 protein.

Wang D ，Zhu X ，Siqin B ，Ren C ，Yi F ... -  《-》

Long Noncoding RNA Cytoskeleton Regulator RNA Suppresses Apoptosis in Hepatoma Cells by Modulating the miR-125a-5p/HS1-Associated Protein X-1 Axis to Induce Caspase-9 Inactivation.

Wu ZY ，Wang Y ，Hu H ，Ai XN ，Zhang Q ，Qin YG ... -  《-》

Long non-coding RNA (lncRNA) CYTOR promotes hepatocellular carcinoma proliferation by targeting the microRNA-125a-5p/LASP1 axis.

Liu Y ，Geng X 《-》

LncRNA CYTOR affects the proliferation, cell cycle and apoptosis of hepatocellular carcinoma cells by regulating the miR-125b-5p/KIAA1522 axis.

Hu B ，Yang XB ，Yang X ，Sang XT ... -  《Aging-US》

LncRNA CYTOR promotes pancreatic cancer cell proliferation and migration by sponging miR-205-5p.

Studies have found that LncRNA CYTOR is an important regulator of cancer. However, the function of lncRNA CYTOR in pancreatic cancer (PC) is unclear. This study amid to explore the regulation of lncRNA CYTOR in PC. The expression of CYTOR and miR-205-5p in PC was detected by RT-qPCR. CCK-8 assay, colony formation assay and scratch test were conducted to detect the effects of CYTOR and miR-205-5p on proliferation and migration of PC cells. Target gene prediction and screening and luciferase reporter assays were used to verify downstream target genes of CYTOR and miR-205-5p. The expression of Cyclin-dependent protein kinase 6 (CDK6) was detected by Western blotting. The tumor growth in mice was detected by in vivo experiments in nude mice. The expression of LncRNA CYTOR was significantly elevated in PC. Knockdown of CYTOR significantly inhibited cell proliferation and migration of PC cells. In vivo animal studies showed that CYTOR promoted tumor growth. MiR-205-5p was a direct target of CYTOR, and the expression levels of miR-205-5p were significantly reduced in PC cell lines. Furthermore, co-transfection of shCYTOR with miR-205-5p inhibitor partially abolished the effect of shCYTOR on cell proliferation and migration. In addition, CYTOR was negatively correlated with the expression of miR-205-5p. CDK6 was a direct target of miR-205-5p, and miR-205-5p mimic and sh CYTOR significantly reduced the expression levels of CDK6. CYTOR can promote PC progression by modulating the miR-205-5p/CDK6 axis, which may be a potential therapeutic target for PC.

Zhu H ，Shan Y ，Ge K ，Lu J ，Kong W ，Jia C ... -  《-》