ABSTRACT
@#[Abstract] Objective: To investigate the effects of miR-361-5p on the oxaliplatin (OXA) resistance of gastric cancer SGC-7901 cells and its mechanism. Methods: The expression of miR-361-5p in gastric cancer cells (MKN-45, MGC80-3 and SGC-7901) and drug-resistant SGC-7901/OXA cells was detected by qPCR. The SGC-7901/OXA cells were transfected with miR-361-5p mimics/inhibitor or sh-CCND1 by using Liposome transfection technology. Then, cell proliferation, apoptosis and cell cycle of SGC-7901/OXA cells were measured by CCK-8 assay and Flow cytometry, respectively. The targeting relationship between miR-361-5p and CCND1 was examined by Dual luciferase report gene assay. The expression level of CCND1 in SGC-7901/OXA cells was detected by WB. Results: miR-361-5p was down-regulated in multiple gastric cancer cells and SGC-7901/OXA cells (P<0.05 or P<0.01). Over-expression of miR-361-5p significantly promoted the apoptosis, induced G0/G1 cell cycle arrest and inhibited cell proliferation of SGC-7901/OXA cells (P<0.05 or P<0.01). Dual luciferase reporter gene results verified that miR-361-5p targeted CCND1 and negatively regulated its expression (P<0.01). Further experiments showed that targeted down-regulation of CCND1 induced apoptosis and G0/G1 cell cycle arrest and inhibited CCND1 expression and proliferation of SGC-7901/OXA cells (P<0.05 or P<0.01). Over-expression of miR-361-5p targetedly down-regulated CCND1 and further promoted cell apoptosis, induced G0/G1 cell cycle arrest and inhibited cell proliferation of SGC-7901/OXA cells (P<0.05 or P<0.01). Conclusion: miR-361-5p over-expression can reverse the resistance of SGC-7901/OXA cells to OXA, and the mechanism may be related to its targeted down-regulation of CCND1 expression.
ABSTRACT
@#[Abstract] Objective: To explore the effect of lncRNA HOTAIR/miR-519d-3p/cyclin D1 (CCND1) axis on the proliferation and metastasis of breast cancer cells and its underlying mechanism. Methods: A total of 50 pairs of breast cancer tissues and corresponding para-cancer tissues resected from breast cancer patients in the Department of Breast Surgery, the Third Hospital of Nanchang from March 2017 to February 2019 were collected for this study. The expression level of HOTAIR in breast cancer tissues and paired paracancer tissues was detected by qPCR, in addition, the expressions of HOTAIR and miR-519d-3p in normal breast epithelial cells and breast cancer cell lines were also detected. Breast cancer SKBR3 cells were divided into NC group (without any treatment), si-HOTAIR group, mir-519d-3p mimics group, miR-519d-3p mimic+pcHOTAIR group, miR-519d-3p mimic+pcCCND1 group, and si-HOTAIR+ pcCCND1 group. The proliferation ability of SKBR3 cells was detected by CCK-8. Invasion and migration of SKBR3 cells were detected by Transwell. The expression levels of E-cadherin, N-cadherin, Vimentin and CCND1 in SKBR3 cells were detected by Western blotting. The targeting relationship between HOTAIR and miR-519d-3p, miR-519d-3p and CCND1 was detected by Dualluciferase reporter gene system. Results: HOTAIR was highly expressed in breast cancer tissues and cell lines, with the highest expression in SKBR3 cells. HOTAIR knockdown significantly inhibited the proliferation, invasion and migration of SKBR3 cells, as well as increased the expression level of E-cadherin and decreased the expression levels of N-cadherin and Vimentin. Dual-luciferase reporter gene assay showed that HOTAIR targetedly down-regulated the expression of miR-519d-3p, and miR-519d-3p targetedly downregulated the expression of CCND1. Further studies showed that knockout of HOTAIR inhibited the EMT, proliferation, invasion and migration of SKBR3 cells through enhancing the inhibitory effect of miR-519d-3p on CCND1 expression (all P<0.05). Conclusion: HOTAIR knockdown inhibits proliferation and metastasis of SKBR3 cells by regulating the axis of miR-519d-3p/CCND1.
ABSTRACT
Objective To investigate the role of miR-203 in radiation-induced thymic lymphoma (RITL).Methods A 60Co irradiator was used for total-body irradiation.MicroRNAs(miRNAs) level was assayed by qRT-PCR.Cell proliferation was assayed by MTT assay.Cell apoptosis was examined by fluorescence activated cell sorter (FACS).Dual luciferase reporter assay system was used to detect the 3'UTR reporter.Results MiR-203 was down-regulated in RITL tissues.Overexpression of miR-203 strongly inhibited the proliferation of both NIH3T3 cells and EL4 cells and vice versa.MiR-203 inhibited cells proliferation and induced apoptosis via TANK-binding kinase (TBK1),SLUG (SNAI2) and Cyclin D1 (CCND1).Conclusions Radiation down-regulated the level of miR-203 in thymic,which promoted radiation-induced thymic lymphoma by targeting TBK1,SNAI2 and CCND1.