Comparative STAT3-Regulated Gene Expression Profile in Renal Cell Carcinoma Subtypes.

Front Oncol

Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, United States.

Published: February 2019

AI Article Synopsis

  • Renal cell carcinomas (RCC) consist of three main subtypes: clear cell, papillary, and chromophobe, each with distinct characteristics.
  • Signal transducer and activator of transcription 3 (STAT3) is often overactive in various cancers, promoting tumor growth and spread, especially in clear cell RCC where its activation is linked to worse outcomes.
  • Research using RNA-seq data from The Cancer Genome Atlas revealed that STAT3 activation predominantly affects clear cell RCC, with several STAT3-regulated genes identified as potential targets for personalized treatment strategies.

Article Abstract

Renal cell carcinomas (RCC) are heterogeneous and can be further classified into three major subtypes including clear cell, papillary and chromophobe. Signal transducer and activator of transcription 3 (STAT3) is commonly hyperactive in many cancers and is associated with cancer cell proliferation, invasion, migration, and angiogenesis. In renal cell carcinoma, increased STAT3 activation is associated with increased metastasis and worse survival outcomes, but clinical trials targeting the STAT3 signaling pathway have shown varying levels of success in different RCC subtypes. Using RNA-seq data from The Cancer Genome Atlas (TCGA), we compared expression of 32 STAT3 regulated genes in 3 RCC subtypes. Our results indicate that STAT3 activation plays the most significant role in clear cell RCC relative to the other subtypes, as half of the evaluated genes were upregulated in this subtype. were upregulated and was downregulated in all three subtypes. Several genes including , and had variable expression in RCC subtypes and are potential therapeutic targets for personalized medicine.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6399114PMC
http://dx.doi.org/10.3389/fonc.2019.00072DOI Listing

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