An epithelial-mesenchymal transition-related long non-coding RNA signature to predict overall survival and immune microenvironment in kidney renal clear cell carcinoma

Bioengineered. 2021 Dec;12(1):555-564. doi: 10.1080/21655979.2021.1880718.

Abstract

Kidney renal clear cell carcinoma (ccRCC) is a malignant tumor originating from renal tubular epithelium, lncRNAs can regulate the occurrence and development of EMT by targeting EMT transcription factors. We constructed a new survival signature based on EMT-related differentially expressed lncRNAs obtained from the Cancer Genome Atlas (TCGA-KIRC). We first determined 1377 EMT-related lncRNAs, lncRNA AL035661.1 with the largest correlation coefficient and the target gene was PFN2 (cor = 0.843; P= 1.37E-146). Meanwhile, we found an AUC of 0.758 in our signature and we predicted the AUC values of the patients' 1, 2, 3-year survival rate as 0.768, 0.749, and 0.762 in TCGA cohort, respectively. Multivariate COX analysis was performed to determine if risk score was an independent prognostic predictor of OS. The results indicated that our risk score can be an independent predictor for OS (Univariate: HR = 1.350, 95% CI = 1.276-1.428, P< 0.001; Multivariate: HR = 1.295, 95% CI = 1.201-1.396, P< 0.001). We identified novel EMT-related lncRNAs markers for ccRCC prognosis. The underlying mechanism between EMT-related lncRNAs in ccRCC and tumor immunity is still unclear and requires further study.

Keywords: Kidney renal clear cell carcinoma; data mining; epithelial-mesenchymal transition; lncRNAs.

MeSH terms

  • Carcinoma, Renal Cell* / genetics
  • Carcinoma, Renal Cell* / metabolism
  • Carcinoma, Renal Cell* / mortality
  • Carcinoma, Renal Cell* / pathology
  • Data Mining
  • Epithelial-Mesenchymal Transition / genetics*
  • Humans
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Neoplasms* / genetics
  • Kidney Neoplasms* / metabolism
  • Kidney Neoplasms* / mortality
  • Kidney Neoplasms* / pathology
  • RNA, Long Noncoding* / analysis
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • Transcriptome / genetics*

Substances

  • RNA, Long Noncoding

Grants and funding

This work is not supported by grants.