{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hu CY"],"funding":["Ministry of Science and Technology, Taiwan","Ditmanson Medical Foundation Chia-Yi Christian Hospital"],"pagination":["104"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9724340"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(1)"],"pubmed_abstract":["<h4>Background</h4>Cisplatin-based chemotherapy is the first line of treatment for bladder cancer. However, cisplatin induces muscle wasting associated with NF-κB and cancer cachexia. HOTAIR, an oncogenic long non-coding RNA (lncRNA), promotes cancer progression in different cancers. Crosstalk between HOTAIR and NF-κB is documented. Prothymosin α (ProT) plays important roles in cancer progression and inflammation. However, the potential link between HOTAIR, ProT, and cisplatin-induced cancer cachexia remains unexplored. Here, we investigated the contribution of HOTAIR in cisplatin-induced cancer cachexia and dissected the potential signaling cascade involving the epidermal growth factor receptor (EGFR), ProT, NF-κB, and HOTAIR.<h4>Materials and methods</h4>Expression of ProT and HOTAIR tra"],"journal":["Journal of biomedical science"],"pubmed_title":["Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer."],"pmcid":["PMC9724340"],"funding_grant_id":["NCKUCYC-P-11101-2","110-2314-B-006-024"],"pubmed_authors":["Shen WT","Shiau AL","Shieh GS","Su BH","Chen SY","Huang WY","Hu CY","Kuo FC","Fu JT","Wang CT","Lee YC","Yang ML","Ou CH","Wu CL","Tsai YS"],"additional_accession":[]},"is_claimable":false,"name":"Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer.","description":"<h4>Background</h4>Cisplatin-based chemotherapy is the first line of treatment for bladder cancer. However, cisplatin induces muscle wasting associated with NF-κB and cancer cachexia. HOTAIR, an oncogenic long non-coding RNA (lncRNA), promotes cancer progression in different cancers. Crosstalk between HOTAIR and NF-κB is documented. Prothymosin α (ProT) plays important roles in cancer progression and inflammation. However, the potential link between HOTAIR, ProT, and cisplatin-induced cancer cachexia remains unexplored. Here, we investigated the contribution of HOTAIR in cisplatin-induced cancer cachexia and dissected the potential signaling cascade involving the epidermal growth factor receptor (EGFR), ProT, NF-κB, and HOTAIR.<h4>Materials and methods</h4>Expression of ProT and HOTAIR tra","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2025-04-19T06:20:19.768Z","creation":"2025-04-19T06:20:19.768Z"},"accession":"S-EPMC9724340","cross_references":{"pubmed":["36471329"],"doi":["10.1186/s12929-022-00887-y"]}}