4.6 Article

LncRNA LINC01537 Promotes Gastric Cancer Metastasis and Tumorigenesis by Stabilizing RIPK4 to Activate NF-kB Signaling

期刊

CANCERS
卷 14, 期 21, 页码 -

出版社

MDPI
DOI: 10.3390/cancers14215237

关键词

lncRNA; LINC01537; gastric cancer; RIPK4; TRIM25; NF-kB

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资金

  1. Natural Science Foundation ofChina [82003253]

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This study revealed that LINC01537 promotes gastric cancer metastasis and tumorigenesis by stabilizing RIPK4 and enhancing the NF-kB signaling pathway expression.
Many studies reported that long noncoding RNAs (lncRNAs) play a critical role in gastric cancer (GC) metastasis and tumorigenesis. However, the underlying mechanisms of lncRNAs in GC remain unexplored to a great extent. LINC01537 expression level was detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). Its biological roles in GC were then investigated using functional experiments. In order to investigate the underlying mechanism of LINC01537 in GC, RNA pull-down, RNA immunoprecipitation, and ubiquitination assays were performed. LINC01537 was significantly overexpressed in GC tissues and associated with a poor prognosis. Functional experimental results revealed that LINC01537 promoted the proliferation, invasion, and migration of GC cells. The animal experiments revealed that LINC01537 promoted tumorigenesis and metastasis in vivo. Mechanistically, LINC01537 stabilizes RIPK4 by reducing the binding of RIPK4 to TRIM25 and reducing its ubiquitination degradation, thereby promoting the expression of the NF-kB signaling pathway. According to our findings, the LINC01537-RIPK4-NF-kB axis promoted GC metastasis and tumorigenesis.

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