SP1 Mediates LMCD1-AS1/let-7b-5p Axis to Promote Epithelial-Mesenchymal Transition of Lung Cancer Cells

Abstract

Background: Considering the oncogenic role of long non-coding RNA (lncRNA) LMCD1-AS1 in various cancers and its dim association with lung cancer (LC), we commence the research to unveil such association. Methods: LMCD1-AS1, let-7b-5p and SP1 expressions in LC cells were predicted by starBase and calculated via quantitative reverse-transcription PCR (qRT-PCR). The targeting relationships were predicted with bioinformatics and further verified using dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay. The effects of LMCD1-AS1 on cell viability (cell counting kit-8), migration, invasion (Transwell assay) and epithelial-mesenchymal transition (EMT, Western blot) were determined with the help of loss- and gain-of-function assay. The regulation of the LMCD1-AS1/let-7b-5p axis on the aforementioned malignant biological behaviors of LC cells and the activation of PI3K/AKT pathway was detected by rescue experiments. Results: LMCD1-AS1 was highly expressed in LC. The malignant biological behaviors and EMT of LC cells were promoted following the overexpression of LMCD1-AS1, but were inhibited by silencing of LMCD1-AS1. SP1 activated the transcription of LMCD1-AS1, and let-7b-5p was the target miRNA of LMCD1-AS1. LMCD1-AS1 regulated the malignant biological behaviors of LC cells and activated PI3K/AKT pathway by targeting let-7b-5p. Conclusions: SP1 mediates LMCD1-AS1 overexpression and promotes the progression of LC by targeting let-7b-5p.