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Bingbing Wang

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Jul 2026

IFFO2 Promotes Tumor Progression and Serves as a Prognostic Biomarker in Liver Hepatocellular Carcinoma

To investigate the role of Intermediate Filament Family Orphan Protein 2 (IFFO2) in Liver Hepatocellular Carcinoma (LIHC), we systematically evaluated mRNA expression and analyzed the correlation between IFFO2 expression and clinicopathological information, patient prognosis, and the immune microenvironment. In this study, the influence of IFFO2 on LIHC proliferation, clone formation, migration, and invasion was demonstrated using in vitro experiments. This will provide a theoretical basis for IFFO2 to be developed into a biomarker and therapeutic target for LIHC. IFFO2 expression in pan-cancer and LIHC tissues was analyzed in the Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases. For assessing diagnostic value, Receiver Operating Characteristic (ROC) curves were used, and Kaplan-Meier (KM) and Cox regression were used for Prognostic analysis. The single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm was used to examine the relationship between IFFO2 expression and immune cell infiltration. In vitro experiments used siRNA to knock down IFFO2 in HUH7 and HepG2 cells, followed by CCK-8 proliferation assays, clone formation, scratch wound-healing assays, transwell invasion assays, and other experiments to examine changes in cellular behavior. IFFO2 expression was obviously upregulated in the LIHC tissues (p < 0.05). The results of the ROC analysis showed a high diagnostic ability, with an Area Under the Curve (AUC) of 0.790. Increased IFFO2 is associated with high pathological stages, high levels of Alpha-Fetoprotein (AFP), prolonged prothrombin time, and shortened overall survival (OS) (p < 0.05). Functional enrichment analysis revealed that IFFO2 is significantly associated with immune regulation, cell cycle, and complement activation pathways. Immune infiltration analysis demonstrated the presence of various immune cell subtypes that exhibited both positive and negative correlations with IFFO2. In vitro experiments have demonstrated that IFFO2 knockdown remarkably diminishes the proliferation, clone formation, migration, and invasion capacities of LIHC cells (p < 0.05). The findings suggest that IFFO2 functions as an oncogene in LIHC. Its strong association with adverse prognosis and its potential to modulate the immune microenvironment underscore its dual potential as a diagnostic biomarker and a promising therapeutic target, warranting further mechanistic and clinical investigation. IFFO2 is significantly upregulated in LIHC and promotes tumor progression; its expression is associated with unfavorable prognostic outcomes, suggesting its potential utility as a biomarker for diagnosis and a therapeutic target.

Qi Li, Shengke Wen, Hong Chen et al. · Current Cancer Therapy Revie... · 0 citations

Open access Aug 2026

Molecular mechanism underlying YibT-mediated RpoS regulation of virulence variation in Salmonella typhimurium.

Salmonella typhimurium, a Gram-negative pathogen widely distributed in the environment, poses a serious threat to public health by contaminating food and causing foodborne diseases. Our preliminary study found that under thymol stress, the expression of YibT, a poorly characterized factor in salmonella, was significantly reduced, and deletion of the yibT gene markedly impaired biofilm formation. However, the biological role of yibT in salmonella pathogenesis remains unclear. In this study, the λ-Red homologous recombination system and pET28a vector were used to construct the single deletion mutant STΔrpoS, the double deletion mutant STΔrpoSΔyibT, complementation strains, and an overexpression strain. Promoter reporter vectors were constructed using pKP302. Growth characteristics, biofilm formation, adhesion, invasion, virulence, and pathogenicity were evaluated. The regulatory relationship between rpoS and yibT was examined by β-galactosidase assays. Results showed that deletion of rpoS and yibT led to slow growth, reduced biofilm formation, and decreased flagella and surface appendages under transmission electron microscopy. qRT-PCRshowed that there is a negative feedback loop between yibT and rpoS, where RpoS positively regulates yibT transcription and YibT negatively regulates RpoS expression. Preliminary detection of β-galactosidase confirms that yibT may be located downstream of rpoS. Cellular infection models demonstrated that deletion of yibT and rpoS significantly reduced salmonella adhesion, invasion, and intracellular survival. In mouse infection experiments, bacterial loads in the liver, spleen, and ileum were markedly decreased in mutant-infected mice, with further reduction under quercetin intervention. Flow cytometry analysis of T-cell subsets suggested attenuated immune modulation by the mutant strains, indicating reduced pathogenicity. Collectively, yibT contributes to regulate adhesion and invasion of S. typhimurium, and its deletion attenuates bacterial virulence and host pathogenicity. YibT may participate in the virulence regulatory network by interacting with the transcriptional regulator RpoS. This study provides a theoretical basis for elucidating the molecular mechanism by which YibT modulates salmonella pathogenicity.

Bingbing Wang, Min Yue, Jianjun Chen et al. · Microbial Pathogenesis · 0 citations