The Hippo transducers TAZ/YAP and their target CTGF in male breast cancer

Oncotarget. 2016 Jul 12;7(28):43188-43198. doi: 10.18632/oncotarget.9668.

Abstract

Male breast cancer (MBC) is a rare disease and its biology is poorly understood. Deregulated Hippo pathway promotes oncogenic functions in female breast cancer. We herein investigated the expression of the Hippo transducers TAZ/YAP and their target CTGF in MBC. Tissue microarrays containing samples from 255 MBC patients were immunostained for TAZ, YAP and CTGF. One hundred and twenty-nine patients were considered eligible. The Pearson's Chi-squared test of independence was used to test the association between categorical variables. The correlation between TAZ, YAP and CTGF was assessed with the Pearson's correlation coefficient. The Kaplan-Meier method and the log-rank test were used for estimating and comparing survival curves. Cox proportional regression models were built to identify variables impacting overall survival. Statistical tests were two-sided. Tumors were considered to harbor active TAZ/YAP-driven gene transcription when they co-expressed TAZ, or YAP, and CTGF. Patients whose tumors had the TAZ/CTGF and YAP/CTGF phenotypes experienced shorter overall survival compared with their negative counterparts (log rank p = 0.036 for both). TAZ/CTGF and YAP/CTGF tumors were associated with decreased survival in patients with invasive ductal carcinomas, G3 tumors, hormone receptor-positive tumors, and tumors with elevated Ki-67. Multivariate analyses confirmed that the TAZ/CTGF and YAP/CTGF phenotypes are independent predictors of survival (HR 2.03, 95% CI: 1.06-3.90, p = 0.033; and HR 2.00, 95% CI: 1.04-3.84, p = 0.037 respectively). Comparable results were obtained when excluding uncommon histotypes (TAZ/CTGF: HR 2.34, 95% CI: 1.16-4.73, p = 0.018. YAP/CTGF. HR 2.36, 95% CI: 1.17-4.77, p = 0.017). Overall, the TAZ/YAP-driven oncogenic program may be active in MBC, conferring poorer survival.

Keywords: Hippo pathway; Hippo transducers; TAZ; YAP; male breast cancer.

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism*
  • Adult
  • Aged
  • Aged, 80 and over
  • Breast Neoplasms, Male / genetics*
  • Breast Neoplasms, Male / mortality
  • Breast Neoplasms, Male / pathology
  • Carcinogenesis / genetics
  • Carcinoma, Ductal, Breast / genetics*
  • Carcinoma, Ductal, Breast / mortality
  • Carcinoma, Ductal, Breast / pathology
  • Connective Tissue Growth Factor / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Hippo Signaling Pathway
  • Humans
  • Immunohistochemistry
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Kaplan-Meier Estimate
  • Ki-67 Antigen / metabolism
  • Male
  • Middle Aged
  • Neoplasm Grading
  • Phenotype
  • Phosphoproteins / metabolism*
  • Proportional Hazards Models
  • Protein Serine-Threonine Kinases / metabolism*
  • Rare Diseases / genetics*
  • Rare Diseases / mortality
  • Rare Diseases / pathology
  • Receptors, Steroid / metabolism
  • Retrospective Studies
  • Signal Transduction / genetics
  • Tissue Array Analysis
  • Trans-Activators
  • Transcription Factors
  • Transcriptional Coactivator with PDZ-Binding Motif Proteins
  • YAP-Signaling Proteins

Substances

  • Adaptor Proteins, Signal Transducing
  • CCN2 protein, human
  • Intracellular Signaling Peptides and Proteins
  • Ki-67 Antigen
  • Phosphoproteins
  • Receptors, Steroid
  • Trans-Activators
  • Transcription Factors
  • Transcriptional Coactivator with PDZ-Binding Motif Proteins
  • WWTR1 protein, human
  • YAP-Signaling Proteins
  • YAP1 protein, human
  • Connective Tissue Growth Factor
  • Protein Serine-Threonine Kinases