Background: Hepatocellular carcinoma (HCC) remains the third leader cancer-associated cause of death globally, but the etiological basis for this complex disease remains poorly clarified. The present study was thus conceptualized to define a prognostic immune-related gene (IRG) signature capable of predicting immunotherapy responsiveness and overall survival (OS) in patients with HCC. Methods: Five differentially expressed IRG associated with HCC were established the immune-related risk model through univariate Cox regression and least absolute shrinkage and selection operator (LASSO) regression analyses. Patients were separated at random into training and testing cohorts, after which the association between the identified IRG signature and OS was evaluated using the “survival” R package. In addition, maftools was leveraged to assess mutational data, with tumor mutation burden (TMB) scores being calculated as follows: (total mutations/total bases) × 106. Immune-related risk term abundance was quantified via “ssGSEA” algorithm using the “gsva” R package. Results: HCC patients were successfully stratified into low-risk and high-risk groups based upon a signature composed of 5 differentially expressed IRGs, with overall survival being significantly different between these 2 groups in training cohort, testing cohort and overall patient cohort ( P = 1.745e-06, P = 1.888e-02, P = 4.281e-07). No association was observed between TMB and this IRG risk score in the overall patient cohort ( P = 0.461). Notably, 19 out of 29 immune-related risk terms differed substantially in the overall patient dataset. These risk terms mainly included checkpoints, human leukocyte antigens, natural killer cells, dendritic cells, and major histocompatibility complex class I. Conclusion: In summary, an immune-related prognostic gene signature was successfully developed and used to predict survival outcomes and immune system status in patients with HCC. This signature has the potential to help guide immunotherapeutic treatment planning for patients affected by this deadly cancer.
Background Epithelial to mesenchymal transition (EMT) is a key process in determining distant metastasis and intra-hepatic dissemination of hepatocellular carcinoma (HCC). Follistatin ( FST ) family members are considered to be an attractive therapeutic targets and prognostic indicators in cancers. As a derivative of FST , Follistatin Like 5 ( FSTL5 ) may play a similar role in HCC cells. This study aimed to investigate the expression and function of FSTL5 in HCC and its role in EMT. Methods FSTL5 , E-cadherin and vimentin in HCC, and paracancerous tissues were detected by immunohistochemistry. Correlation of FSTL5 expression with overall survival was assessed. The proliferation and invasion of HCC cell lines SK-Hep1 and MHCC-LM3 were analyzed by cell counting kit-8 and Transwell assays. The expression of FSTL5 , E-cadherin, and vimentin in HCC cells was examined by polymerase chain reaction and Western blot analysis. T -test was used to analyze the difference in proliferation and invasion ability between groups. The Spearman rank correlation test was used to detect the correlation between the expression of FSTL5 and E-cadherin or vimentin. Results The expression of FSTL5 in HCC was lower than that in paracancerous tissues (9.97% vs . 82.55%, χ 2 = 340.15, P < 0.001). Patients with high FSTL5 expression had a better prognosis ( χ 2 = 8.22, P = 0.004) and smaller tumor diameter ( χ 2 = 45.52, P < 0.001), less lymph node metastasis ( χ 2 = 5.58, P = 0.02), earlier tumor node metastasis stage ( χ 2 = 11.29, P = 0.001), a reduced number of tumors ( χ 2 = 5.05, P = 0.02), lower alpha-fetoprotein value ( χ 2 = 24.36, P < 0.001), more probability of hepatitis carrying ( χ 2 = 40.9, P < 0.001), and better liver function grade ( χ 2 = 5.21, P = 0.02). Immunohistochemistry showed that FSTL5 expression in HCC tissues was positively correlated with E-cadherin expression ( r = 0.38, ...
Hepatocellular carcinoma is a common malignant tumor and the third most common cause of cancer-related deaths. In this study, we selected H2AFY as a potential oncogene from three online databases, and verified differential expression between normal and liver cancer tissues. Moreover, H2AFY expression was significantly correlated with the clinical characteristics and the survival of liver cancer patients. H2AFY expression was correlated with poor prognosis of liver cancer patients. H2AFY expression was also significantly higher in liver cancer cells. Knockdown and overexpression of H2AFY in liver cancer cells showed that H2AFY promoted the proliferation and clone formation of liver cancer cells but had no significant effects on the migration and invasion ability of liver cancer cells. Western blot analysis, immunohistochemistry, and immunofluorescence double staining confirmed that H2AFY upregulated LC3 and p62 expression in liver cancer tissues and cells. In conclusion, H2AFY is highly expressed in liver cancer cells and tissues, and promotes the proliferation and autophagy of liver cancer cells. H2AFY is a potential target for liver cancer therapy. Abbreviations : APLF: aprataxin pnk-like factor; HCC: Hepatocellular carcinoma; H2AFY: H2A histone family member Y
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