Fig. 4: CCDC91 exerts its pro-tumor function via the LDHA-related aerobic glycolysis pathway.

A Upregulation of CCDC91 expression was positively correlated with activated glycolysis metabolic pathways in HCC as predicted by GSEA from TCGA dataset (GSEA, gene set enrichment analysis; NES, normalized enrichment score, pā<ā0.001). B The volcano graph showing the differentially expression genes (DEGs; |log2FCā|āā„ 1, pāā¤ā0.05) identified by RNA-seq between HepG2-CCDC91 and HepG2-VC cells. C The top 20 pathways revealed by KEGG enrichment analysis of DEGs. D Glucose levels were detected in CCDC91-overexpressing HCC cells and control cells (nā=ā3). E Lactate levels were detected in CCDC91-overexpressing HCC cells and control cells (nā=ā3). F The mRNA level of the key glycolysis differential expressed genes in CCDC91-overexpressing HCC cells and control cells by qPCR (nā=ā3). G The protein level of LDHA in CCDC91-overexpressing HCC cells and control cells by western blot (nā=ā3). H Correlation analysis of CCDC91 and LDHA levels in HCC tissues using the data from TCGA database. I Immunohistochemistry staining and analysis showed the protein expression of LDHA in HCC tissues and matched non-cancerous liver tissues (nā=ā80). J The KaplanāMeier analysis revealed the association of LDHA with the overall survival of HCC patients from TMA cohort (nā=ā80). K Correlation analysis of CCDC91 and LDHA levels in HCC tissues using the data from TMA cohort (nā=ā80). Statistical analysis was performed using Studentās t test in (D, E, F, and I). Data represents meanā±āSEM. *, pā<ā0.05; **, pā<ā0.01; ***, pā<ā0.001.