ArticleCancer cell international2026
Shared molecular mechanisms of common differentially expressed genes (C-DEGs) linking gallbladder stones to carcinogenesis: integrated bioinformatics and experimental validation.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionGallbladder stones (GBS) and gallbladder cancer (GBC) are prevalent gallbladder diseases that, while presenting distinct clinical manifestations, may share common regulatory mechanisms at the molecular level. This study aimed to identify and validate common differentially expressed genes (C-DEGs) in GBS and GBC through comprehensive bioinformatics analysis and experimental validation to elucidate potential molecular pathological mechanisms linking these two conditions.
methodsWe analyzed gene expression data from publicly available databases for GBS and GBC, identifying 94 common differentially expressed genes (C-DEGs) through differential expression analysis. Gene ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to characterize the functions and pathways associated with these genes. Furthermore, we examined the differential expression of transcription factors (TFs) in both GBS and GBC groups and experimentally validated the functions of these genes.
resultsOur analysis identified 94 C-DEGs, including 10 hub genes (HC-DEGs): SOCS3, GADD45B, SGK1, MYC, HBEGF, KLF10, EGF, IL6, NR4A3, and CDKN1A. GO functional analysis revealed that these genes primarily regulate smooth muscle cell proliferation, animal organ regeneration, peptidyl-tyrosine phosphorylation, epidermal growth factor-activated receptor activity, and the JAK-STAT signaling pathway. KEGG pathway analysis demonstrated their involvement in multiple cancers (bladder, endometrial, colorectal, thyroid, breast, and gastric), the FoxO signaling pathway, the JAK-STAT signaling pathway, the ErbB signaling pathway, and transcriptional dysregulation in cancer. Additionally, we identified 14 differentially expressed TFs in the GBS group and 11 in the GBC group. Four transcription factors—E2F1, ETS2, EZH2, and MYC—showed differential co-expression in both conditions and were jointly involved in regulating two hub genes (CDKN1A and MYC). DISCUSSION: Through comprehensive bioinformatics analysis and experimental validation, this study revealed common molecular mechanisms between GBS and GBC. We identified and validated 10 hub genes that exhibited significant differential expression in both conditions and were primarily involved in multiple cancer-related signaling pathways. Furthermore, we identified four transcription factors (E2F1, ETS2, EZH2, and MYC) showing differential co-expression in both GBS and GBC, which jointly regulated two hub genes (CDKN1A and MYC). These findings illuminate shared molecular mechanisms between GBS and GBC, providing novel insights for further investigation of their molecular pathological mechanisms and establishing an important theoretical foundation for future preventive and therapeutic strategies.
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