Long intergenic non‐coding RNA Linc00485 promotes lung cancer progression by modulating miR‐298/c‐Myc axis

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 ca...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2021-01, Vol.25 (1), p.309-322
Main Authors: Zhang, Zhenyang, Lin, Wenwei, Lin, Yuhan, Kang, Mingqiang, Zhu, Jiafu, Tong, Zhangwei, Wu, Long, Sun, Jianhai, Lin, Jiangbo
Format: Article
Language:English
Subjects:
Biotechnology
Cell adhesion & migration
Cell proliferation
Colorectal cancer
c‐Myc
Experiments
Flow cytometry
Gene expression
Humidity
Invasiveness
Laboratories
Linc00485
Lung cancer
Medical diagnosis
Medical research
Metastases
Metastasis
MicroRNAs
miR‐298
Myc protein
Non-coding RNA
Original
Ovarian cancer
Penicillin
Phenotypes
siRNA
Tumors
Xenografts
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Summary: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.
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.16036