RESUMO
Objective: The aim of the present study was to construct a prognostic model based on the peptidyl prolyl cis-trans isomerase gene signature and explore the prognostic value of this model in patients with hepatocellular carcinoma. Methods: The transcriptome and clinical data of hepatocellular carcinoma patients were downloaded from The Cancer Genome Atlas and the International Cancer Genome Consortium database as the training set and validation set, respectively. Peptidyl prolyl cis-trans isomerase gene sets were obtained from the Molecular Signatures Database. The differential expression of peptidyl prolyl cis-trans isomerase genes was analyzed by R software. A prognostic model based on the peptidyl prolyl cis-trans isomerase signature was established by Cox, Lasso, and stepwise regression methods. Kaplan-Meier survival analysis was used to evaluate the prognostic value of the model and validate it with an independent external data. Finally, nomogram and calibration curves were developed in combination with clinical staging and risk score. Results: Differential gene expression analysis of hepatocellular carcinoma and adjacent tissues showed that there were 16 upregulated genes. A prognostic model of hepatocellular carcinoma was constructed based on three gene signatures by Cox, Lasso, and stepwise regression analysis. The Kaplan-Meier curve showed that hepatocellular carcinoma patients in high-risk score group had a worse prognosis (p < 0.05). The receiver operating characteristic curve revealed that the area under curve values of predicting the survival rate at 1, 2, 3, 4, and 5 years were 0.725, 0.680, 0.644, 0.630, and 0.639, respectively. In addition, the evaluation results of the model by the validation set were basically consistent with those of the training set. A nomogram incorporating clinical stage and risk score was established, and the calibration curve matched well with the diagonal. Conclusion: A prognostic model based on 3 peptidyl prolyl cis-trans isomerase gene signatures is expected to provide reference for prognostic risk stratification in patients with hepatocellular carcinoma.
RESUMO
Background: Autophagy plays an important role in the development of cancer. However, the prognostic value of autophagy-related genes (ARGs) in cervical cancer (CC) is unclear. The purpose of this study is to construct a survival model for predicting the prognosis of CC patients based on ARG signature. Methods: ARGs were obtained from the Human Autophagy Database and Molecular Signatures Database. The expression profiles of ARGs and clinical data were downloaded from the TCGA database. Differential expression analysis of CC tissues and normal tissues was performed using R software to screen out ARGs with an aberrant expression. Univariate Cox, Lasso, and multivariate Cox regression analyses were used to construct a prognostic model which was validated by using the test set and the entire set. We also performed an independent prognostic analysis of risk score and some clinicopathological factors of CC. Finally, a clinical practical nomogram was established to predict individual survival probability. Results: Compared with normal tissues, there were 63 ARGs with an aberrant expression in CC tissues. A risk model based on 3 ARGs was finally obtained by Lasso and Cox regression analysis. Patients with high risk had significantly shorter overall survival (OS) than low-risk patients in both train set and validation set. The ROC curve validated its good performance in survival prediction, suggesting that this model has a certain extent sensitivity and specificity. Multivariate Cox analysis showed that the risk score was an independent prognostic factor. Finally, we mapped a nomogram to predict 1-, 3-, and 5-year survival for CC patients. The calibration curves indicated that the model was reliable. Conclusion: A risk prediction model based on CHMP4C, FOXO1, and RRAGB was successfully constructed, which could effectively predict the prognosis of CC patients. This model can provide a reference for CC patients to make precise treatment strategy.