Bioinformatic analysis suggests that UGT2B15 activates the Hippo‑YAP signaling pathway leading to the pathogenesis of gastric cancer

Oncol Rep. 2018 Oct;40(4):1855-1862. doi: 10.3892/or.2018.6604. Epub 2018 Jul 26.

Abstract

Gastric cancer (GC) is one of the most common malignancies that threatens human health. As the molecular mechanisms unerlying GC are not completely understood, identification of genes related to GC could provide new insights into gene function as well as potential treatment targets. We discovered that UGT2B15 may contribute to the pathogenesis and progression of GC using GEO data and bioinformatic analysis. Using TCGA data, UGT2B15 mRNA was found to be significantly overexpressed in GC tissues; patients with higher UGT2B15 had a poorer prognosis. It was further discovered that UGT2B15 and FOXA1 were both upregulated, and UGT2B15 and Foxa1 were positively correlated in GC. It is known that Foxa1 is a vital threshold to activate the Hippo‑YAP signaling pathway. In addition, we suggest that a potential molecular mechanisms includes UGT2B15 which may upregulate Foxa1, activate the Hippo‑YAP signaling pathway and contribute to the development of GC. Taken together, our findings demonstrate that UGT2B15 may be an oncogene in GC and is a promising therapeutic target for cancer treatment.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Apoptosis
  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism*
  • Case-Control Studies
  • Cell Proliferation
  • Computational Biology / methods*
  • Female
  • Follow-Up Studies
  • Gene Expression Regulation, Neoplastic
  • Glucuronosyltransferase / genetics
  • Glucuronosyltransferase / metabolism*
  • Hepatocyte Nuclear Factor 3-alpha / genetics
  • Hepatocyte Nuclear Factor 3-alpha / metabolism*
  • Hippo Signaling Pathway
  • Humans
  • Male
  • Middle Aged
  • Phosphoproteins / genetics
  • Phosphoproteins / metabolism*
  • Prognosis
  • Protein Interaction Maps
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Signal Transduction
  • Stomach Neoplasms / genetics
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology*
  • Survival Rate
  • Transcription Factors
  • Tumor Cells, Cultured
  • YAP-Signaling Proteins

Substances

  • Adaptor Proteins, Signal Transducing
  • Biomarkers, Tumor
  • FOXA1 protein, human
  • Hepatocyte Nuclear Factor 3-alpha
  • Phosphoproteins
  • Transcription Factors
  • YAP-Signaling Proteins
  • YAP1 protein, human
  • Glucuronosyltransferase
  • UDP-glucuronosyltransferase 2B15, human
  • Protein Serine-Threonine Kinases