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pmid:34123804
LINC00467 Promotes Tumor Progression via Regulation of the NF-kb Signal Axis in Bladder Cancer.
Jiawei Xiao · Lian Gong · Mengqing Xiao · Dong He · Liang Xiang · Zhanwang Wang · Yaxin Cheng · Liping Deng · Ke Cao
Frontiers in oncology · 2021 doi:10.3389/fonc.2021.652206
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Experiment
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Complete file
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In this study, we found that LINC00467 was significantly highly expressed in bladder cancer through bioinformatic analysis. The present study aimed to explore the role of LINC00467 in bladder cancer and its possible underlying molecular mechanisms.\nMETHODS: The expression of LINC00467 was obtained from GEO (GSE31189), the TCGA database, and qRT-PCR. The role of LINC00467 in bladder cancer was assessed both in vitro and in vivo. RIP, RNA pulldown, and CO-IP were used to demonstrate the potential mechanism by which LINC00467 regulates the progression of bladder cancer.\nRESULTS: Through the analysis of GEO (GSE133624) and the TCGA database, it was found that LINC00467 was highly expressed in bladder cancer tissues and that the expression of LINC00467 was significantly negatively correlated with patient prognosis. Cell and animal experiments suggest that LINC00467 promotes the proliferation and invasion of bladder cancer cells. On the one hand, LINC00467 can directly bind to NF-kb-p65 mRNA to stabilize its expression. On the other hand, LINC00467 can directly bind to NF-kb-p65 to promote its translocation into the nucleus to activate the NF-κB signaling pathway, which promotes the progression of bladder cancer.\nCONCLUSIONS: LINC00467 is highly expressed in bladder cancer and can promote the progression of bladder cancer by regulating the NF-κB signaling pathway. 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