{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Seo SU"],"funding":["Keimyung University","National Research Foundation of Korea (NRF)","Keimyung University (KMU)","National Research Foundation of Korea"],"pagination":["115"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8816936"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(2)"],"pubmed_abstract":["Cathepsin D (Cat D) is well known for its roles in metastasis, angiogenesis, proliferation, and carcinogenesis in cancer. Despite Cat D being a promising target in cancer cells, effects and underlying mechanism of its inhibition remain unclear. Here, we investigated the plausibility of using Cat D inhibition as an adjuvant or sensitizer for enhancing anticancer drug-induced apoptosis. Inhibition of Cat D markedly enhanced anticancer drug-induced apoptosis in human carcinoma cell lines and xenograft models. The inhibition destabilized Bcl-xL through upregulation of the expression of RNF183, an E3 ligase of Bcl-xL, via NF-κB activation. Furthermore, Cat D inhibition increased the proteasome activity, which is another important factor in the degradation of proteins. Cat D inhibition resulted "],"journal":["Cell death & disease"],"pubmed_title":["Cathepsin D as a potential therapeutic target to enhance anticancer drug-induced apoptosis via RNF183-mediated destabilization of Bcl-xL in cancer cells."],"pmcid":["PMC8816936"],"funding_grant_id":["2020 Scholar Research Grant","NRF-2019R1A2C2005921","NRF-2021R1A4A1029238","NRF-2020R1C1C1009889"],"pubmed_authors":["Seo SU","Lee HS","Min KJ","Kim SH","Woo SM","Jang Y","Nam JO","Gabrielson E","Im SS","Lee H","Han E","Kwon TK"],"additional_accession":[]},"is_claimable":false,"name":"Cathepsin D as a potential therapeutic target to enhance anticancer drug-induced apoptosis via RNF183-mediated destabilization of Bcl-xL in cancer cells.","description":"Cathepsin D (Cat D) is well known for its roles in metastasis, angiogenesis, proliferation, and carcinogenesis in cancer. Despite Cat D being a promising target in cancer cells, effects and underlying mechanism of its inhibition remain unclear. Here, we investigated the plausibility of using Cat D inhibition as an adjuvant or sensitizer for enhancing anticancer drug-induced apoptosis. Inhibition of Cat D markedly enhanced anticancer drug-induced apoptosis in human carcinoma cell lines and xenograft models. The inhibition destabilized Bcl-xL through upregulation of the expression of RNF183, an E3 ligase of Bcl-xL, via NF-κB activation. Furthermore, Cat D inhibition increased the proteasome activity, which is another important factor in the degradation of proteins. Cat D inhibition resulted ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-05-31T02:03:21.047Z","creation":"2025-04-06T12:10:05.233Z"},"accession":"S-EPMC8816936","cross_references":{"pubmed":["35121737"],"doi":["10.1038/s41419-022-04581-7"]}}