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LncRNA CALML3-AS1 modulated by m6A modification induces BTNL9 methylation to drive non-small-cell lung cancer progression.
Zhang, Heng; Wang, Shao-Qiang; Zhu, Jie-Bo; Wang, Li-Na; Lin, Hang; Li, Lin-Feng; Cheng, Yuan-Da; Duan, Chao-Jun; Zhang, Chun-Fang.
Afiliación
  • Zhang H; Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China. 404346@csu.edu.cn.
  • Wang SQ; Xiangya Lung Cancer Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China. 404346@csu.edu.cn.
  • Zhu JB; National Clinical Research Center for Geriatric Disorders (Xiangya Hospital), Changsha, 410008, Hunan Province, P. R. China. 404346@csu.edu.cn.
  • Wang LN; Department of Thoracic Surgery, Weifang People's Hospital, Weifang Medical University, Weifang, 261041, Shandong Province, P.R. China.
  • Lin H; Department of Scientific Research Management, Weifang People's Hospital, Weifang Medical University, Weifang, 261041, Shandong Province, P.R. China.
  • Li LF; Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
  • Cheng YD; Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Jining, 272029, Shandong Province, P. R. China.
  • Duan CJ; Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
  • Zhang CF; Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
Cancer Gene Ther ; 30(12): 1649-1662, 2023 12.
Article en En | MEDLINE | ID: mdl-37884580
Non-small cell lung cancer (NSCLC) is a common and lethal malignancy. The carcinogenic roles of lncRNA CALML3 antisense RNA 1 (CALML3-AS1) have been documented. However, the function and potential mechanisms of CALML3-AS1 in the progression of NSCLC need to be further explored. The molecule expression was assessed by qRT-PCR and Western blot. The subcellular localization of CALML3-AS1 was observed by fluorescence in situ hybridization (FISH). The malignant behaviors of NSCLC cells were evaluated by CCK-8, colony formation, EdU, wound healing and transwell assays. In vivo xenograft tumor and liver metastatic models were established. The molecular mechanisms were investigated by RIP, RNA pull-down and ChIP assays. The methylation level was detected by MSP. Herein, we found that CALML3-AS1 was upregulated, while butyrophilin-like 9 (BTNL9) was downregulated in NSCLC. Functionally, CALML3-AS1 depletion repressed NSCLC cell malignant phenotypes, in vivo tumor growth, and liver metastasis. Mechanistically, AlkB homolog 5 (ALKBH5) enhanced CALML3-AS1 stability via N6-methyladenosine (m6A) demethylation, whereas m6A reader YTH domain-containing 2 (YTHDC2) destabilized CALML3-AS1. Moreover, CALML3-AS1 inhibited BTNL9 transcription and expression through the recruitment of Zeste homolog 2 (EZH2). Rescue experiments demonstrated that BTNL9 downregulation counteracted sh-CALML3-AS1-mediated antitumor effects on NSCLC. Taken together, CALML3-AS1 modulated by ALKBH5 and YTHDC2 in an m6A modification dependent manner drives NSCLC progression via epigenetically repressing BTNL9.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / MicroARNs / ARN Largo no Codificante / Metilación de ARN / Neoplasias Pulmonares Límite: Humans Idioma: En Revista: Cancer Gene Ther Asunto de la revista: GENETICA MEDICA / NEOPLASIAS / TERAPEUTICA Año: 2023 Tipo del documento: Article Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / MicroARNs / ARN Largo no Codificante / Metilación de ARN / Neoplasias Pulmonares Límite: Humans Idioma: En Revista: Cancer Gene Ther Asunto de la revista: GENETICA MEDICA / NEOPLASIAS / TERAPEUTICA Año: 2023 Tipo del documento: Article Pais de publicación: Reino Unido