4.6 Article

LINC00467 Promotes Tumor Progression via Regulation of the NF-kb Signal Axis in Bladder Cancer

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FRONTIERS IN ONCOLOGY
卷 11, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.652206

关键词

LINC00467; NF-kb; proliferation; invasion; bladder cancer

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资金

  1. National Natural Science Foundation of China [81874137]
  2. Hunan Province Science and Technology Talent Promotion Project [2019TJ-Q10]
  3. Wisdom Accumulation and Talent Cultivation Project of the Third Xiangya Hospital of Central South University [ZC060001]
  4. Independent Exploration and Innovation Project of Central South University [2020zzts897]

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The study found that LINC00467 is highly expressed in bladder cancer and can promote the progression of bladder cancer by regulating the NF-kappa B signaling pathway. Targeting LINC00467 may provide a new strategy for the treatment of bladder cancer and improve patient prognosis.
Purpose Long non-coding RNAs (lncRNAs) play an important role in the occurrence and development of bladder cancer, but the underlying molecular mechanisms remain largely unknown. 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. Methods 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. Results 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-kappa B signaling pathway, which promotes the progression of bladder cancer. Conclusions LINC00467 is highly expressed in bladder cancer and can promote the progression of bladder cancer by regulating the NF-kappa B signaling pathway. Therefore, targeting LINC00467 is very likely to provide a new strategy for the treatment of bladder cancer and for improving patient prognosis.

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