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Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer

Hu, Che-Yuan ; Su, Bing-Hua ; Lee, Ya-Che ; Wang, Chung-Teng ; Yang, Mei-Lin ; Shen, Wan-Ting ; Fu, Jing-Ting ; Chen, Shih-Yao ; Huang, Wei-Yun ; Ou, Chien-Hui ; Tsai, Yuh-Shyan ; Kuo, Feng-Chih ; Shiau, Ai-Li ; Shieh, Gia-Shing ; Wu, Chao-Liang

Journal of biomedical science, 2022-12, Vol.29 (1), p.104-104, Article 104 [Periódico revisado por pares]

England: BioMed Central Ltd

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Título:
Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer
Autor: Hu, Che-Yuan ; Su, Bing-Hua ; Lee, Ya-Che ; Wang, Chung-Teng ; Yang, Mei-Lin ; Shen, Wan-Ting ; Fu, Jing-Ting ; Chen, Shih-Yao ; Huang, Wei-Yun ; Ou, Chien-Hui ; Tsai, Yuh-Shyan ; Kuo, Feng-Chih ; Shiau, Ai-Li ; Shieh, Gia-Shing ; Wu, Chao-Liang
Assuntos: Analysis ; Animals ; Antineoplastic Agents - adverse effects ; Antineoplastic Agents - therapeutic use ; Atrophy ; Bladder ; Bladder cancer ; Cachexia ; Cachexia - chemically induced ; Cachexia - genetics ; Cancer ; Cancer therapies ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Chemotherapy ; Cisplatin ; Cisplatin - adverse effects ; Cisplatin - therapeutic use ; Cytokines ; Development and progression ; DNA damage ; EGFR ; Epidermal growth factor ; Epidermal growth factor receptors ; ErbB Receptors - metabolism ; Genes ; Growth factors ; Health services ; HOTAIR ; Humans ; Inflammation ; Inhibitors ; Kinases ; Medical prognosis ; Metabolic disorders ; Metastasis ; Mice ; Muscles ; Muscular Atrophy - chemically induced ; Muscular Atrophy - genetics ; Myoblasts ; NF-kappa B - genetics ; NF-kappa B - metabolism ; NF-κB protein ; Non-coding RNA ; Phosphorylation ; Prothymosin α ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Roles ; Sarcopenia ; Signal Transduction ; Signaling ; Signs and symptoms ; Therapeutic targets ; Tumor cell lines ; Tumors ; Urinary Bladder Neoplasms - drug therapy
É parte de: Journal of biomedical science, 2022-12, Vol.29 (1), p.104-104, Article 104
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Descrição: 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. Expression of ProT and HOTAIR transcripts and their correlations in tumor tissues of bladder cancer patients and bladder cancer cell lines were determined by RT-qPCR. Next, levels of phospho-EGFR, EGFR, phospho-NF-κB, and NF-κB were examined by immunoblot analysis in human bladder cancer cells treated with cisplatin. Expression of HOTAIR in cisplatin-treated cells was also assessed by RT-qPCR. Pharmacological inhibitors and overexpression and knockdown approaches were exploited to decipher the signaling pathway. The murine C2C12 myoblasts were used as an in vitro muscle atrophy model. The syngeneic murine MBT-2 bladder tumor was used to investigate the role of mouse Hotair in cisplatin-induced cancer cachexia. Expression of ProT and HOTAIR was higher in bladder tumors than in normal adjacent tissues. There were positive correlations between ProT and HOTAIR expression in clinical bladder tumors and bladder cancer cell lines. Cisplatin treatment increased EGFR and NF-κB activation and upregulated ProT and HOTAIR expression in bladder cancer cells. ProT overexpression increased, whereas ProT knockdown decreased, HOTAIR expression. Notably, cisplatin-induced HOTAIR upregulation was abrogated by EGFR inhibitors or ProT knockdown. ProT-induced HOTAIR overexpression was diminished by NF-κB inhibitors. HOTAIR overexpression enhanced, whereas its knockdown reduced, cell proliferation, cachexia-associated pro-inflammatory cytokine expression, and muscle atrophy. Cachexia-associated symptoms were ameliorated in mice bearing Hotair-knockdown bladder tumors undergoing cisplatin treatment. We demonstrate for the first time a critical role for HOTAIR and identify the involvement of the EGFR-ProT-NF-κB-HOTAIR signaling axis in cisplatin-induced cachexia in bladder cancer and likely other cancers. Our findings also provide therapeutic targets for this disease.
Editor: England: BioMed Central Ltd
Idioma: Inglês

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Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer

Hu, Che-Yuan ; Su, Bing-Hua ; Lee, Ya-Che ; Wang, Chung-Teng ; Yang, Mei-Lin ; Shen, Wan-Ting ; Fu, Jing-Ting ; Chen, Shih-Yao ; Huang, Wei-Yun ; Ou, Chien-Hui ; Tsai, Yuh-Shyan ; Kuo, Feng-Chih ; Shiau, Ai-Li ; Shieh, Gia-Shing ; Wu, Chao-Liang

England: BioMed Central Ltd

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