Frontiers in Cell and Developmental Biology (Jan 2022)

A Novel Platelet-Related Gene Signature for Predicting the Prognosis of Triple-Negative Breast Cancer

  • Jindong Xie,
  • Yutian Zou,
  • Feng Ye,
  • Wanzhen Zhao,
  • Wanzhen Zhao,
  • Xinhua Xie,
  • Xueqi Ou,
  • Xiaoming Xie,
  • Weidong Wei

DOI
https://doi.org/10.3389/fcell.2021.795600
Journal volume & issue
Vol. 9

Abstract

Read online

Regarded as the most invasive subtype, triple-negative breast cancer (TNBC) lacks the expression of estrogen receptors (ERs), progesterone receptors (PRs), and human epidermal growth factor receptor 2 (HER2) proteins. Platelets have recently been shown to be associated with metastasis of malignant tumors. Nevertheless, the status of platelet-related genes in TNBC and their correlation with patient prognosis remain unknown. In this study, the expression and variation levels of platelet-related genes were identified and patients with TNBC were divided into three subtypes. We collected cohorts from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases. By applying the least absolute shrinkage and selection operator (LASSO) Cox regression method, we constructed a seven-gene signature which classified the two cohorts of patients with TNBC into low- or high-risk groups. Patients in the high-risk group were more likely to have lower survival rates than those in the low-risk group. The risk score, incorporated with the clinical features, was confirmed as an independent factor for predicting the overall survival (OS) time. Functional enrichment analyses revealed the involvement of a variety of vital biological processes and classical cancer-related pathways that could be important to the ultimate prognosis of TNBC. We then built a nomogram that performed well. Moreover, we tested the model in other cohorts and obtained positive outcomes. In conclusion, platelet-related genes were closely related to TNBC, and this novel signature could serve as a tool for the assessment of clinical prognosis.

Keywords