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Insulin-Like Growth Factor Binding Protein 5-A Probable Target of Kidney Renal Papillary Renal Cell Carcinoma

Shuqiang Wang1, Quan Hong1, Xiaodong Geng1

  • 1Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases, China.

Biomed Research International
|December 31, 2019
PubMed

Insights

Insulin-like growth factor binding protein 5 (IGFBP5) is downregulated in kidney renal papillary renal cell carcinoma (KIRP). Lower IGFBP5 expression correlates with poorer survival, suggesting IGFBP5 as a potential therapeutic target for KIRP.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Kidney renal papillary cell carcinoma (KIRP) represents 10-15% of renal cell carcinoma (RCC) cases.
  • Existing targeted therapies show limited efficacy in advanced KIRP, highlighting the urgent need for novel therapeutic targets.
  • Insulin-like growth factor (IGF) binding protein 5 (IGFBP5) is a secreted protein involved in cell proliferation, adhesion, migration, inflammation, and fibrosis, independent of IGF signaling.

Purpose of the Study:

  • To investigate the expression patterns and functional significance of IGFBP5 in KIRP.
  • To identify potential upstream regulatory factors influencing IGFBP5 expression in KIRP.
  • To evaluate IGFBP5 as a potential therapeutic target for KIRP.

Main Methods:

  • Utilized The Cancer Genome Atlas (TCGA) database for expression analysis of IGFBP5 in KIRP tissues versus control tissues.
  • Performed bioinformatic analysis to identify biological processes and pathways associated with altered IGFBP5 expression.
  • Validated the regulatory roles of VEGFA and TGF-β on IGFBP5 expression in the Caki-2 cell line.

Main Results:

  • IGFBP5 expression was found to be significantly downregulated in KIRP kidney tissues compared to normal kidney tissues.
  • A negative correlation was observed between IGFBP5 expression levels and patient survival in KIRP.
  • Bioinformatic analysis implicated pathways such as blood vessel development, cellular response to growth factors, TGF-β signaling, and extracellular matrix organization in altered IGFBP5 expression.
  • VEGFA and TGF-β were identified as probable upstream regulatory factors of IGFBP5, with experimental validation in the Caki-2 cell line.

Conclusions:

  • IGFBP5 is downregulated in KIRP and its reduced expression is associated with poorer patient outcomes.
  • Altered IGFBP5 expression in KIRP is linked to key cellular processes including angiogenesis and extracellular matrix remodeling.
  • VEGFA and TGF-β likely play regulatory roles in controlling IGFBP5 expression in KIRP.
  • IGFBP5 presents a promising candidate for a novel therapeutic target in kidney renal papillary cell carcinoma.

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