Integrative Analysis of Non-coding RNAs and Hippo Signaling Pathway in Hepatocellular Carcinoma Using Bioinformatics and Experimental Approaches
Loading...
Date
2025-01-11
0000-0003-3707-7581 Journal Title
Journal ISSN
Volume Title
Publisher
Brieflands
Abstract
Background: Hepatocellular carcinoma (HCC) is one of the most prevalent and lethal malignancies globally. Non-coding RNAs (ncRNAs) are pivotal in regulating gene expression and cancer progression, yet their precise functions within HCC pathways remain elucidated. Objectives: To investigate the role of ncRNAs in regulating key genes involved in Hippo signaling and HCC pathways and to identify potential novel regulatory mechanisms in HCC progression. Methods: Gene expression data from the GEO database (GSE14520) were analyzed for expression changes of LEF1, MOB1A, PRKCB, and SMARCA2 in HCC. Physical interactions between selected ncRNAs (lnc-LRR1-1:1, lnc-LRR1-1:2, and hsa_circ_0001380) and target mRNAs were predicted, using the long non-coding RNA-target analysis resource (LncTAR) tool. miRNA analysis was performed to identify potential competing endogenous RNA (ceRNA) mechanisms. qPCR analysis in HCC cell lines was conducted for experimental validation. Results: Significant upregulation of LEF1 and downregulation of PRKCB were observed in HCC samples. The strongest predicted interactions were identified between lnc-LRR1-1:2 and MOB1A isoforms. miRNA analysis suggested that the studied ncRNAs could act as ceRNAs. qPCR analysis confirmed upregulation of hsa_circ_0001380 and slight downregulation of lnc-LRR1-1:1,2 in HCC cell lines. Conclusions: This study unveils a complex regulatory network, where ncRNAs can modulate the expression of key genes in HCC. The predicted interactions, particularly between lnc-LRR1-1:2 and MOB1A, and between hsa_circ_0001380 and hsa-miR-193b-3p suggest novel regulatory mechanisms in HCC progression. These findings provide new insights into the role of ncRNAs in HCC pathogenesis and identify potential avenues for future research and targeted therapies.