Lnc-BM通过FASTK/MT-ND6轴调节线粒体呼吸功能促进胃癌进展OACSTPCD

Objective To explore the role and molecular mechanism of Lnc-BM in the occurrence and development of gastric cancer(GC).Methods GC tissues and paired adjacent normal tissues of 36 GC patients were collected,and the expression of Lnc-BM was detected by RT-qPCR.Colony formation and CCK-8 assays were used to investigate the proliferation of GC cells.The migration and invasion properties of GC cells were investigated via Transwell assay.RNA pull-down assay was applied to confirm the interaction between FASTK and Lnc-BM.Western blot assay was used to detect FASTK protein level in Lnc-BM overexpressing or knockdown cells.Mitochondrial respiratory capacity and the related proteins expression levels were detected by Seahorse and Western blot assays,respectively.Lnc-BM stably overexpressing GC cells were constructed and then injected subcutaneously into nude mice.The tumor growth was observed.Results Lnc-BM was highly expressed in GC tissues compared with their paired adjacent normal tissues.Lnc-BM overexpression significantly promoted GC cells proliferation migration and invasion,while Lnc-BM knockdown inhibited GC cells proliferation,migration and invasion(P<0.05).RNA pull-down experiment demonstrated that Lnc-BM can directly bind to FASTK.Western blot results indicated that overexpression of Lnc-BM increased the protein levels of FASTK,while knockdown of Lnc-BM inhibited the expression of FASTK(P<0.05).Compared to the control group,overexpression of Lnc-BM increased the levels of mitochondria associated proteins,such as MT-ND6 and TOM20(P<0.05).Seahorse results indicated that overexpression of Lnc-BM enhanced mitochondrial respiratory capacity(P<0.05).Knocking down FASTK in Lnc-BM stably overexpressing cells can reverse the increase in mitochondrial respiratory capacity caused by Lnc-BM overexpression(P<0.05).In vivo,the results of subcutaneously implanted tumor model in nude mouse showed that Lnc-BM overexpression promoted the tumor growth(P<0.05).Conclusion Lnc-BM promotes GC progression by regulating mitochondrial respiratory function through the FASTK/MT-ND6 axis.