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A novel biomarker NIFK-AS1 promotes hepatocellular carcinoma cell cycle progression through interaction with . | LitMetric

Background: Hepatocellular carcinoma (HCC) is one of the most common carcinomas all over the world, with high mortality and low survival rate. Notably, many studies have showed that a variety of molecules play vital roles in the progression of HCC. Therefore, it is urgent to find reliable biomarkers to diagnose HCC and developing novel strategies are required for the effective treatment of patients with HCC.

Methods: This study obtained an HCC cohort from The Cancer Genome Atlas (TCGA). For prognostic analysis, the TCGA cohort was grouped according to different median boundaries. The key module associated with HCC was adopted by Weighted Gene Co-expression Network analysis (WGCNA). We also analyzed the survival ability, functional enrichment, and potential binding proteins of key lncRNAs. The expression of hub lncRNAs in HCC tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell Counting Kit-8 (CCK-8) and flow cytometry were applied to detect the cell proliferation, apoptosis, and cell cycle. The interaction between and SRSF1 was examined using an RNA pull-down assay.

Results: The green module is the key module in HCC. was highly expressed in HCC tissues and correlated with a poor prognosis in HCC patients (P=0.008). was also significantly associated with cell mitosis, the cell cycle, and other biological processes. deletion prevented cell proliferation, induced apoptosis, caused G2/M arrest, and affected cell cycle progression. RNA pull-down validated the interaction. The overexpression of was sufficient to rescue the growth of knockdown HepG2 cells.

Conclusions: This study suggested that promotes HCC cell cycle progression through interaction with and its findings provide new insights into therapeutic targets for HCC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9459191PMC
http://dx.doi.org/10.21037/jgo-22-705DOI Listing

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