The crucial role
of competitive endogenous RNA (ceRNA)
in the malignant
biological behavior of tumors has been certificated. Nevertheless,
the detailed function and molecular mechanism of ceRNA associated
with cuproptosis in hepatocellular carcinoma (HCC) remains dismal.
In this study, we first constructed a protein–protein interaction
network and identified the module with the highest degree of aggregation
degree. DLAT and PDHA1 were screened out of the module after differential
expression and survival analysis. Next, we reverse-predicted the upstream
miRNA and lncRNA from mRNA (DLAT, PDHA1) and successfully established
the ceRNA network-SNHG3/miR-1306-5p/PDHA1. SNHG3 was identified to
be an independent prognostic biomarker based on the outcome of univariate
and multivariate Cox analyses. Subsequently, we implemented methylation,
immune infiltration, and drug sensitivity analysis to investigate
the potential biological functions of SNHG3 in HCC. In addition, SNHG3
expression was upregulated in liver cancer cell lines. In vitro functional
assay revealed that SNHG3 knockdown significantly attenuated proliferation,
migration, and invasion of liver cancer cells. In summary, SNHG3 exhibited
oncogenic characterization via sponging miR-1306-5p to regulate PDHA1,
which might function as a promising prognostic indicator and a potential
therapeutic target for HCC and shed new light on the molecular mechanism
of HCC progression.