Background: Recently, numerous studies have demonstrated the emerging role of long non-coding RNAs (lncRNAs) in human cancers. Linc00467 is a newly defined lncRNA and was reported to promote cell survival in neuroblastoma. However, the function of linc00467 in lung cancer is still unclear.
Material and methods: We analyzed linc00467 expression and survival data derived from The Cancer Genome Altas lung adenocarcinoma (LUAD) dataset as well as in collected LUAD tissues. Then, we silenced linc00467 expression in two lung cancer cell lines using small interfering RNAs and explored the effect of linc00467 knockdown on cell growth in vitro and in vivo. Moreover, we revealed a novel target gene of linc00467 and elucidated the underlying competitive endogenous RNA regulatory mechanism in lung cancer cells.
Results: Our data suggested that linc00467 expression was elevated in LUAD tissues and correlated with overall survival of LUAD patients. Linc00467 knockdown resulted in reduced proliferation rate in lung cancer cells. Furthermore, we elucidated that linc00467 promoted CCND1 expression in lung cancer cells via functioning as a molecular sponge for miR-20b-5p.
Conclusion: Linc00467/miR-20b-5p/CCND1 signaling pathway may provide new insights into lung cancer treatment.
Keywords: CCND1; cell growth; linc00467; lung adenocarcinoma; miR-20b-5p.
© 2019 Ding et al.