Open Access

ARTICLE

Angiogenic Gene PTK2 is a Potential Biomarker of Gestational Diabetes Mellitus and is Significantly Associated with Breast Cancer Immune Infiltration

Xuelian Du^1,#, Hao Shi^2,#, Haiyan Liu¹, Linghua Zhou¹, Anqun Xie¹, Jufang Guo^1,*

1 Department of Obstetrics and Gynecology, Jinniu District Maternal and Child Health Hospital, Chengdu, 610000, China
2 Department of Pediatrics, Jinniu District Maternal and Child Health Hospital, Chengdu, 610000, China

* Corresponding Author: Jufang Guo. Email:
# These authors contributed equally to this work and should be considered co-first authors

Oncologie 2022, 24(4), 769-787. https://doi.org/10.32604/oncologie.2022.026248

Received 26 August 2022; Accepted 24 October 2022; Issue published 31 December 2022

Abstract

Background: Gestational diabetes mellitus (GDM) affects the health of numerous women around the world. A recent study has shown that GDM is associated with an increased incidence of cancer. In this study, we aimed to explore the possible shared mechanisms and potential common therapeutic targets between GDM and cancer. Methods: The limma package was used to identify differentially expressed genes (DEGs) in GDM. The Cytoscape plugin cytoHubba was used to screen hub genes. The CIBERSORT algorithm was used to explore the correlation between hub genes and immunity. Cox regression analysis was used to assess the relationship between protein tyrosine kinase 2 (PTK2) expression and prognosis in pan-cancer. Single-sample gene set enrichment analysis (ssGSEA) and CIBERSORT were used to assess the correlation between PTK2 and immunity in cancer. Mutation and methylation analyses of PTK2 were assessed using Spearman’s correlation test. Results: A total of 871 DEGs were identified, among which the hub genes were significantly highly expressed in GDM and had a strong association with immunity. Pan-cancer analysis revealed that PTK2 was significantly overexpressed in multiple types of cancer. Survival analysis showed that PTK2 was significantly associated with poor prognosis in multiple cancers. Mutational analysis revealed that copy number variation of PTK2 mediated abnormal expression of mRNA, and expression of PTK2 was significantly correlated with tumor mutational burden of various cancers. Immune correlation analysis showed pre-correlation of PTK2 with breast cancer, and patients with low expression of PTK2 could benefit more from immunotherapy. GSEA enrichment analysis was enriched in adaptive immune response, which verified the strong association of PTK2 with immunity in breast cancer. Conclusions: PTK2 was involved in the immune response of GDM and breast cancer and may be a novel clinical prognostic marker and potential common therapeutic target for GDM and breast cancer.

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