Construction and validation of a prognostic model for overall survival time of patients with ovarian cancer by metabolism‐related genes

Author:

Kong Deshui12,Guo Hongyan12ORCID

Affiliation:

1. Department of Obstetrics and Gynecology Peking University Third Hospital Beijing China

2. National Clinical Research Center for Obstetrics and Gynecology (Peking University Third Hospital) Beijing China

Abstract

AbstractBackgroundOvarian cancer is a female‐specific malignancy with high morbidity and mortality. The metabolic reprogramming of tumor cells is closely related to the biological behavior of tumors.MethodsThe prognostic signature of the metabolism‐related gene (MRGs) was established by LASSO‐Cox regression analysis. The prognostic signature of MRGs was also prognosticated in each clinical subgroup. These genes were subjected to functional enrichment analysis and tissue expression exploration. Analysis of the MRG prognostic signature in terms of immune cell infiltration and antitumor drug susceptibility was also performed.ResultsA MRG prognostic signature including 21 genes was established and validated. Most of the 21 MRGs were expressed at different levels in ovarian cancer than in normal ovarian tissue. The enrichment analysis suggested that MRGs were involved in lipid metabolism, membrane organization, and molecular binding. The MRG prognostic signature demonstrated the predictive value of overall survival time in various clinical subgroups. The monocyte, NKT, Tgd and Tex cell scores showed differences between the groups with high‐ and low‐risk score. The antineoplastic drug analysis we performed provided information on ovarian cancer drug therapy and drug resistance. In vitro experiments verified that PLCH1 in 21 MRGs can regulate the apoptosis and proliferation of ovarian cancer cells.ConclusionThis metabolism‐related prognostic signature was a potential prognostic factor in patients with ovarian cancer, demonstrating high stability and accuracy.

Funder

Capital Health Research and Development of Special Fund

Publisher

Wiley

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