Functional data link LINC02163 expression to HCC cell growth, PI3K/AKT pathway activity, and changes in stemness-related markers, although the underlying mechanism remains to be established.
Abstract
Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality worldwide and has a poor prognosis. Long non-coding RNAs (lncRNAs) are important regulators of cancer biology; however, the expression pattern, clinical significance, and biological relevance of LINC02163 in HCC remain insufficiently characterized.
We examined LINC02163 expression in the TCGA‒LIHC cohort and verified its expression by qRT-PCR in an independent clinical cohort. Prognostic significance was assessed using Kaplan–Meier and Cox regression analyses. Functional effects were evaluated by CCK-8, colony formation, and xenograft assays. Exploratory enrichment analysis, Western blotting, and RNA‒FISH were then used to explore related pathways, stemness-related markers, PI3K/AKT activity, and subcellular localization. We also built an exploratory prognostic nomogram combining LINC02163 expression with clinicopathological variables.
LINC02163 expression was significantly upregulated in HCC tissues and cell lines; higher expression was associated with shorter overall survival. Silencing LINC02163 reduced cell proliferation and clonogenic growth and was accompanied by slower xenograft growth, whereas overexpression produced the opposite pattern in vitro. RNA‒FISH showed that LINC02163 was mainly cytoplasmic. Changes in LINC02163 expression were also accompanied by alterations in stemness-related markers and PI3K/AKT phosphorylation. In the TCGA‒LIHC development cohort, the exploratory nomogram showed apparent discrimination for 1-, 3-, and 5-year OS.
LINC02163 may represent a candidate prognostic biomarker in HCC. The functional data also link LINC02163 expression to HCC cell growth, PI3K/AKT pathway activity, and changes in stemness-related markers, although the underlying mechanism remains to be established.
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BACKGROUND
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METHODS
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