{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo K"],"funding":["National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund)","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["48"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9905489"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(1)"],"pubmed_abstract":["Although dysregulated HMMR is linked to prostate cancer (PCa) prognosis, the precise mechanisms remain unclear. Here, we sought to elucidate the role of HMMR in PCa progression as well as underlying mechanism. Herein, we found that upregulation of HMMR frequently observed in PCa samples and was associated with poor prognosis. Additionally, HMMR significantly promoted PCa proliferation and metastasis through gain- and loss-of function approaches in vitro and in vivo. Mechanistically, HMMR may interact with AURKA and elevated AURKA protein level through inhibiting ubiquitination-mediated degradation, which subsequently activated mTORC2/AKT pathway to ensure the reinforcement of PCa progression. Moreover, upregulated E2F1 caused from sustained activation of mTORC2/AKT pathway in turn function"],"journal":["Cell death discovery"],"pubmed_title":["HMMR promotes prostate cancer proliferation and metastasis via AURKA/mTORC2/E2F1 positive feedback loop."],"pmcid":["PMC9905489"],"funding_grant_id":["82072841"],"pubmed_authors":["Tang Z","Xu K","Guo K","Li Z","Luo J","Gao Z","Liu C","Lai C","Shi J","Li K"],"additional_accession":[]},"is_claimable":false,"name":"HMMR promotes prostate cancer proliferation and metastasis via AURKA/mTORC2/E2F1 positive feedback loop.","description":"Although dysregulated HMMR is linked to prostate cancer (PCa) prognosis, the precise mechanisms remain unclear. Here, we sought to elucidate the role of HMMR in PCa progression as well as underlying mechanism. Herein, we found that upregulation of HMMR frequently observed in PCa samples and was associated with poor prognosis. Additionally, HMMR significantly promoted PCa proliferation and metastasis through gain- and loss-of function approaches in vitro and in vivo. Mechanistically, HMMR may interact with AURKA and elevated AURKA protein level through inhibiting ubiquitination-mediated degradation, which subsequently activated mTORC2/AKT pathway to ensure the reinforcement of PCa progression. Moreover, upregulated E2F1 caused from sustained activation of mTORC2/AKT pathway in turn function","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-07-14T17:05:43.93Z","creation":"2025-04-04T23:52:16.178Z"},"accession":"S-EPMC9905489","cross_references":{"pubmed":["36750558"],"doi":["10.1038/s41420-023-01341-0"]}}