<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hu CY</submitter><funding>Ministry of Science and Technology, Taiwan</funding><funding>Ditmanson Medical Foundation Chia-Yi Christian Hospital</funding><pagination>104</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9724340</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>29(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Materials and methods&lt;/h4>Expression of ProT and HOTAIR tra</pubmed_abstract><journal>Journal of biomedical science</journal><pubmed_title>Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer.</pubmed_title><pmcid>PMC9724340</pmcid><funding_grant_id>NCKUCYC-P-11101-2</funding_grant_id><funding_grant_id>110-2314-B-006-024</funding_grant_id><pubmed_authors>Shen WT</pubmed_authors><pubmed_authors>Shiau AL</pubmed_authors><pubmed_authors>Shieh GS</pubmed_authors><pubmed_authors>Su BH</pubmed_authors><pubmed_authors>Chen SY</pubmed_authors><pubmed_authors>Huang WY</pubmed_authors><pubmed_authors>Hu CY</pubmed_authors><pubmed_authors>Kuo FC</pubmed_authors><pubmed_authors>Fu JT</pubmed_authors><pubmed_authors>Wang CT</pubmed_authors><pubmed_authors>Lee YC</pubmed_authors><pubmed_authors>Yang ML</pubmed_authors><pubmed_authors>Ou CH</pubmed_authors><pubmed_authors>Wu CL</pubmed_authors><pubmed_authors>Tsai YS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Materials and methods&lt;/h4>Expression of ProT and HOTAIR tra</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-19T06:20:19.768Z</modification><creation>2025-04-19T06:20:19.768Z</creation></dates><accession>S-EPMC9724340</accession><cross_references><pubmed>36471329</pubmed><doi>10.1186/s12929-022-00887-y</doi></cross_references></HashMap>