ArticleOncotarget2016
The Hippo transducers TAZ/YAP and their target CTGF in male breast cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Oestrogen receptor phosphorylation profiles and in silico PAM50 subtyping reflect sexual dimorphism in breast cancer.The journal of pathology. Clinical research · 2026Article
- Lysophosphatidic acid mediates skeletal muscle fibrosis in denervation via activation of YAP/TAZ.JCI insight · 2026Article
- Advances in the treatment of glioma-related signaling pathways and mechanisms by metformin.Frontiers in oncology · 2025Review
- YAP1 expression in colorectal cancer confers the aggressive phenotypes via its target genes.Cell cycle (Georgetown, Tex.) · 2024Article
- Episodic Binge-like Ethanol Reduces Skeletal Muscle Strength Associated with Atrophy, Fibrosis, and Inflammation in Young Rats.International journal of molecular sciences · 2023Article
- Article
- Dysregulation of the Scribble/YAP/β-catenin axis sustains the fibroinflammatory response in a PKHD1FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Hippo/TEAD4 signaling pathway as a potential target for the treatment of breast cancer.Oncology letters · 2021Review
- The Role of the Hippo Pathway in Breast Cancer Carcinogenesis, Prognosis, and Treatment: A Systematic Review.Breast care (Basel, Switzerland) · 2021Review
- The regulatory networks of the Hippo signaling pathway in cancer development.Journal of Cancer · 2021Review
- Rab14 Overexpression Promotes Proliferation and Invasion Through YAP Signaling in Non-Small Cell Lung Cancers.OncoTargets and therapy · 2020Article
- Article
- Down-regulation of interferon regulatory factor 2 binding protein 2 suppresses gastric cancer progression by negatively regulating connective tissue growth factor.Journal of cellular and molecular medicine · 2019Article
- MicroRNA‑608 sensitizes non‑small cell lung cancer cells to cisplatin by targeting TEAD2.Molecular medicine reports · 2019Article
- [YAP1 knockdown suppresses the proliferation, migration and invasion of human nasopharyngeal carcinoma cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- STARD13-correlated ceRNA network-directed inhibition on YAP/TAZ activity suppresses stemness of breast cancer via co-regulating Hippo and Rho-GTPase/F-actin signaling.Journal of hematology & oncology · 2018Article
- Expression of the Hippo transducer TAZ in association with WNT pathway mutations impacts survival outcomes in advanced gastric cancer patients treated with first-line chemotherapy.Journal of translational medicine · 2018Article
- Article
- Analysis of the ATR-Chk1 and ATM-Chk2 pathways in male breast cancer revealed the prognostic significance of ATR expression.Scientific reports · 2017Article
- Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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