miR-133b inhibits cell proliferation, migration, and invasion of lung adenocarcinoma by targeting CDCA8.

Lung adenocarcinoma (LUAD) is the most common type of lung cancer. This study aims to explore the mechanism by which CDCA8 regulates cell proliferation, invasion, and migration of LUAD, and to generate novel insights into targeted therapy of LUAD. Expression profiles of mature microRNAs (miRNAs) and mRNAs, along with clinical data of LUAD were downloaded from TCGA database for differential analysis and survival analysis to mine differentially expressed mRNAs. qRT-PCR was used to detect the expression of CDCA8 and miR-133b in LUAD cell lines, and western blot was used to detect protein expression. The effects of CDCA8 on the proliferation, migration, and invasion of LUAD cells were detected by CCK-8 assay, scratch healing assay, and Transwell assay. Bioinformatics predicted the target miRNA of CDCA8, and dual-luciferase reporter gene assay was used to verify the binding relationship between miR-133b and CDCA8. Data from TCGA-LUAD showed that CDCA8 was significantly overexpressed in LUAD tissue, while its upstream miRNA (miR-133b) was significantly lowly expressed. The result of dual-luciferase test showed that miR-133b targeted CDCA8. The results of in vitro functional experiments showed that overexpression of CDCA8 could promote the proliferation, invasion, and migration of LUAD cells, and miR-133b could reverse this promotion by targeting CDCA8. This study found that CDCA8 was a carcinogenic factor in LUAD cells and it was regulated by upstream miR-133b. miR-133b could inhibit proliferation, invasion, and migration of LUAD cells by targeting CDCA8.

Hu C ，Wu J ，Wang L ，Liu X ，Da B ，Liu Y ，Huang L ，Chen Q ，Tong Y ，Jiang Z ... -  《-》

miR-139-5p Inhibits Lung Adenocarcinoma Cell Proliferation, Migration, and Invasion by Targeting MAD2L1.

miR-139-5p is lowly expressed in various human cancers and exerts its antitumor effect through different molecular mechanisms, yet the molecular mechanism of miR-139-5p in lung adenocarcinoma (LUAD) remains to be further elucidated. The study is aimed at investigating the role and the regulatory mechanism of miR-139-5p in LUAD progression. Differential analysis was performed on miRNA expression data in the TCGA-LUAD dataset. qRT-PCR was employed to detect the transcription levels of miR-139-5p and MAD2L1 in LUAD cells, while western blot was carried out for the detection of MAD2L1 protein expression. CCK-8 and Transwell assays were implemented to assess LUAD cell proliferation, migration, and invasion. A dual-luciferase reporter gene assay was conducted to verify the direct targeting relationship between miR-139-5p and MAD2L1. miR-139-5p was significantly downregulated in LUAD cells in comparison with that in human normal bronchial epithelial cells. Overexpressing miR-139-5p inhibited LUAD cell proliferation, migration, and invasion, while opposite results could be observed when miR-139-5p was inhibited. MAD2L1 was identified as a direct target of miR-139-5p in LUAD. Besides, the inhibitory effect of miR-139-5p overexpression on LUAD cell proliferation, migration, and invasion was attenuated by overexpressing MAD2L1. Our study suggests that miR-139-5p is lowly expressed in LUAD cells and inhibits LUAD cell proliferation, migration, and invasion by targeted suppressing MAD2L1 expression. It is of potential significance for the prognosis and treatment of LUAD.

Li J ，He X ，Wu X ，Liu X ，Huang Y ，Gong Y ... -  《-》

miR-186-5p promotes cell growth, migration and invasion of lung adenocarcinoma by targeting PTEN.

Feng H ，Zhang Z ，Qing X ，French SW ，Liu D ... -  《-》

miR-21-5p promotes lung adenocarcinoma cell proliferation, migration and invasion via targeting WWC2.

Wang G ，Zhou Y ，Chen W ，Yang Y ，Ye J ，Ou H ，Wu H ... -  《-》

CircPRKCI regulates proliferation, migration and cycle of lung adenocarcinoma cells by targeting miR-219a-5p-regulated CAMK1D.

Sui MH ，Zhang WW ，Geng DM ，Sun DJ ... -  《-》