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Long intergenic non-coding RNA Linc00485 promotes lung cancer progression by modulating miR-298/c-Myc axis.
Zhang, Zhenyang; Lin, Wenwei; Lin, Yuhan; Kang, Mingqiang; Zhu, Jiafu; Tong, Zhangwei; Wu, Long; Sun, Jianhai; Lin, Jiangbo.
Afiliación
  • Zhang Z; Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
  • Lin W; Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
  • Lin Y; School of Stomatology, Fujian Medical University, Fuzhou, Fujian, China.
  • Kang M; Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
  • Zhu J; Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
  • Tong Z; Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
  • Wu L; Department of Pathology, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
  • Sun J; Department of Oncology, Hubei No. 3 People's Hospital of Jianghan University, Wuhan, Hebei, China.
  • Lin J; Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
J Cell Mol Med ; 25(1): 309-322, 2021 01.
Article en En | MEDLINE | ID: mdl-33237626
ABSTRACT
Long non-coding RNAs (lncRNAs), which are non-protein-coding transcripts, are emerging as novel biomarkers for cancer diagnosis. Their dysregulation is increasingly recognized to contribute to the development and progression of human cancers, including lung cancer. Linc00485 is a newly discovered cancer-related lncRNA; however, little is known about its role in lung cancer progression. In this study, we found that the expression of Linc00485 was significantly increased in human lung cancer tissue and associated with malignant phenotypes, including tumour-node-metastasis (TNM) stage, metastasis and relapse. Furthermore, the proliferative, migratory and invasive abilities of lung cancer cells in vitro were significantly enhanced by overexpression of Linc00485 but inhibited by its silencing. Mechanistically, Linc00485 regulated the expression of c-Myc by directly binding to miR-298; the effects of Linc00485 overexpression could be significantly reversed by a c-Myc inhibitor or small interfering RNA. Xenotransplantation experiments showed that Linc00485 silencing significantly weakened the proliferation potential of A549 cells in vivo. Overall, these findings indicate that Linc00485 overexpression down-regulates miR-298, resulting in the up-regulation of c-Myc and thereby promoting the development of lung cancer.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Proteínas Proto-Oncogénicas c-myc / Proteínas Proto-Oncogénicas c-myb / MicroARNs / Neoplasias Pulmonares Límite: Female / Humans / Male / Middle aged Idioma: En Revista: J Cell Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2021 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Proteínas Proto-Oncogénicas c-myc / Proteínas Proto-Oncogénicas c-myb / MicroARNs / Neoplasias Pulmonares Límite: Female / Humans / Male / Middle aged Idioma: En Revista: J Cell Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2021 Tipo del documento: Article País de afiliación: China