{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhu M"],"funding":["U.S. Department of Health & Human Services | NIH | National Cancer Institute","NCI NIH HHS"],"pagination":["6049-6056"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8526415"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["40(41)"],"pubmed_abstract":["Yes-associated protein 1 (YAP1), a key player in the Hippo pathway, has been shown to play a critical role in tumor progression. However, the role of YAP1 in prostate cancer cell invasion, migration, and metastasis is not well defined. Through functional, transcriptomic, epigenomic, and proteomic analyses, we showed that prolyl hydroxylation of YAP1 plays a critical role in the suppression of cell migration, invasion, and metastasis in prostate cancer. Knockdown (KD) or knockout (KO) of YAP1 led to an increase in cell migration, invasion, and metastasis in prostate cancer cells. Microarray analysis showed that the EMT pathway was activated in Yap1-KD cells. ChIP-seq analysis showed that YAP1 target genes are enriched in pathways regulating cell migration. Mass spectrometry analysis identif"],"journal":["Oncogene"],"pubmed_title":["P4HA2-induced prolyl hydroxylation suppresses YAP1-mediated prostate cancer cell migration, invasion, and metastasis."],"pmcid":["PMC8526415"],"funding_grant_id":["P30 CA016672","R01 CA174798","R00 CA194289","P50 CA140388"],"pubmed_authors":["Jain AK","Park J","Liang X","Song JH","Chang Q","Peng R","Logothetis CJ","Hanash S","Ma X","Mak CSL","Zheng SE","Wang G","Lin SH","Lan Z","Zhu M","Tang M","Hou P","Huang A","Katayama H","Chen R"],"additional_accession":[]},"is_claimable":false,"name":"P4HA2-induced prolyl hydroxylation suppresses YAP1-mediated prostate cancer cell migration, invasion, and metastasis.","description":"Yes-associated protein 1 (YAP1), a key player in the Hippo pathway, has been shown to play a critical role in tumor progression. However, the role of YAP1 in prostate cancer cell invasion, migration, and metastasis is not well defined. Through functional, transcriptomic, epigenomic, and proteomic analyses, we showed that prolyl hydroxylation of YAP1 plays a critical role in the suppression of cell migration, invasion, and metastasis in prostate cancer. Knockdown (KD) or knockout (KO) of YAP1 led to an increase in cell migration, invasion, and metastasis in prostate cancer cells. Microarray analysis showed that the EMT pathway was activated in Yap1-KD cells. ChIP-seq analysis showed that YAP1 target genes are enriched in pathways regulating cell migration. Mass spectrometry analysis identif","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2025-04-04T10:27:39.048Z","creation":"2025-02-19T01:21:27.1Z"},"accession":"S-EPMC8526415","cross_references":{"pubmed":["34471235"],"doi":["10.1038/s41388-021-02000-3"]}}