ArticleOncogene2015
In vivo quantitative phosphoproteomic profiling identifies novel regulators of castration-resistant prostate cancer growth.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 78 citations in OpenAlex.
- Review
- Activation of the Hippo Pathway by ATN Suppresses Cancer Stem-Like Properties and EGFR-Associated Signaling in Castration-Resistant Prostate Cancer CellsInternational journal of medical sciences · 2026Article
- Elevated VRK1 levels after androgen deprivation therapy promote prostate cancer progression by upregulating YAP1 expression.Journal of cancer research and clinical oncology · 2025Article
- Regulation of Cancer Metastasis by PAK2.International journal of molecular sciences · 2024Review
- Adipose Tissues Have Been Overlooked as Players in Prostate Cancer Progression.International journal of molecular sciences · 2024Review
- Article
- Investigating High-risk Factors, Precise Diagnosis, and Treatment of Castration- Resistant Prostate Cancer (CRPC).Combinatorial chemistry & high throughput screening · 2024Article
- YAP is required for prostate development, regeneration, and prostate stem cell function.Cell death discovery · 2023Article
- Deregulated kinase action in prostate cancer: molecular basis and therapeutic implications.Endocrine-related cancer · 2023Review
- Aspartoacylase suppresses prostate cancer progression by blocking LYN activation.Military Medical Research · 2023Article
- Integrative Analysis of Transcriptome, Proteome, and Phosphoproteome Reveals Potential Roles of Photosynthesis Antenna Proteins in Response to Brassinosteroids Signaling in Maize.Plants (Basel, Switzerland) · 2023Article
- TPM2 attenuates progression of prostate cancer by blocking PDLIM7-mediated nuclear translocation of YAP1.Cell & bioscience · 2023Article
- Advancements in Oncoproteomics Technologies: Treading toward Translation into Clinical Practice.Proteomes · 2023Review
- The Extracellular Matrix Stiffening: A Trigger of Prostate Cancer Progression and Castration Resistance?Cancers · 2022Review
- From Omics to Multi-Omics Approaches for In-Depth Analysis of the Molecular Mechanisms of Prostate Cancer.International journal of molecular sciences · 2022Review
- Review
- The Hippo pathway in cancer: YAP/TAZ and TEAD as therapeutic targets in cancer.Clinical science (London, England : 1979) · 2022Review
- Emerging Proteins in CRPC: Functional Roles and Clinical Implications.Frontiers in oncology · 2022Review
- Review
- Bidirectional Cross-talk between MAOA and AR Promotes Hormone-Dependent and Castration-Resistant Prostate Cancer.Cancer research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer remains a leading cause of cancer-related mortality worldwide owing to our inability to treat effectively castration-resistant tumors. To understand the signaling mechanisms sustaining castration-resistant growth, we implemented a mass spectrometry-based quantitative proteomic approach and use it to compare protein phosphorylation in orthotopic xenograft tumors grown in either intact or castrated mice. This investigation identified changes in phosphorylation of signaling proteins such as MEK, LYN, PRAS40, YAP1 and PAK2, indicating the concomitant activation of several oncogenic pathways in castration-resistant tumors, a notion that was confirmed by tumor transcriptome analysis. Further analysis demonstrated that the activation of mTORC1, PAK2 and the increased levels of YAP1 in castration-resistant tumors can be explained by the loss of androgen inhibitory actions. The analysis of clinical samples demonstrated elevated levels of PAK2 and YAP1 in castration-resistant tumors, whereas knockdown experiments in androgen-independent cells demonstrated that both YAP1 and PAK2 regulate cell colony formation and cell invasion activity. PAK2 also influenced cell proliferation and mitotic timing. Interestingly, these phenotypic changes occur in the absence of obvious alterations in the activity of AKT, MAPK or mTORC1 pathways, suggesting that PAK2 and YAP1 may represent novel targets for the treatment of castration-resistant prostate cancer. Pharmacologic inhibitors of PAK2 (PF-3758309) and YAP1 (Verteporfin) were able to inhibit the growth of androgen-independent PC3 xenografts. This work demonstrates the power of applying high-resolution mass spectrometry in the proteomic profiling of tumors grown in vivo for the identification of novel and clinically relevant regulatory proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.