Lung cancer as one of the commonest invasive malignancies is featured by high morbidity and mortality, wherein lung adenocarcinoma (LUAD) is the most prevalent subtype. Accumulating evidence exhibited that microRNAs are involved in LUAD occurrence and progression. In this study, miR-182-5p was observed to increase in both LUAD tissue and cell lines. Overexpression of miR-182-5p could prominently facilitate cell proliferation, migration, and invasion in LUAD. Through bioinformatics analysis, STARD13 was theorized as the target gene of miR-182-5p, which was lowly expressed in LUAD. Further molecular experiments manifested that miR-182-5p bound to the 3 ′ -untranslated region of STARD13, and there was an inverse correlation between STARD13 and miR-182-5p in LUAD. Rescue experiments demonstrated that silencing STARD13 conspicuously restored the inhibitory effect of decreased miR-182-5p on cell proliferation, migration, and invasion in LUAD. Together, our findings revealed novel roles of the miR-182-5p/STARD13 axis in LUAD progression.

Objective: We aimed to investigate the mechanism of the regulatory axis of miR-196b/AQP4 underlying the invasion and migration of lung adenocarcinoma (LUAD) cells. Methods: LUAD miRNA and mRNA expression profiles were downloaded from TCGA database and then differential analysis was used to identify the target miRNA. Target gene for the miRNA was obtained via prediction using 3 bioinformatics databases and intersection with the differentially expressed mRNAs searched from TCGA-LUAD. Then, qRT-PCR and western blot were used to validate the expression of miR-196b and AQP4. Dual-luciferase reporter assay was performed to confirm the targeting relationship between miR-196b and AQP4. Transwell assay was used to investigate the migration and invasion of LUAD cells. Results: MiR-196b was screened out by differential and survival analyses, and the downstream target gene AQP4 was identified. In LUAD, miR-196b was highly expressed while AQP4 was poorly expressed. Besides, overexpression of miR-196b promoted cell invasion and migration, while overexpression of AQP4 had negative effects. Moreover, the results of the dual-luciferase reporter assay suggested that AQP4 was a direct target of miR-196b. In addition, we also found that overexpressing AQP4 could suppress the promotive effect of miR-196b on cancer cell invasion and migration. Conclusion: MiR-196b promotes the invasion and migration of LUAD cells by down-regulating AQP4, which helps us find new molecular targeted therapies for LUAD.

Purpose: To explore regulatory mechanism of miR-129-2-3p underlying esophageal carcinoma (EC) cell progression and generate new ideas for targeted treatment of EC. Methods: Mature miRNA expression data and total RNA sequencing data of EC in TCGA-ESCA dataset were utilized to explore differentially expressed miRNAs (DEmiRNAs). StarBase database was then utilized to predict targets of miRNA. MiR-129-2-3p and DNMT3B expression in EC cell lineswas assayed through qRT-PCR and Western blot. CCK-8, scratch healing and transwell assays were conducted to assess the impact of miR-129-2-3p on EC cell phenotypes. In addition, dual-luciferase assay was completed to identify binding relationship between DNMT3B and miR-129-2-3p. Results: MiR-129-2-3p was noticeably less expressed in EC tissue, while DNMT3B was highly expressed. MiR-129-2-3p could bind to DNMT3B. Furthermore, in vitro functional experiments uncovered that overexpressed miR-129-2-3p repressed EC cell dysregulation of is often confirmed in solid tumors. Xiao Y et al.[18] discovered that miR-129-2 affects invasion and proliferation of lung cancer cells. Similarly, Wang D et al.[19] found that miR-129-1-3p constrains gastric cancer cell migration via modulating BDKRB2. However, there has been no research reported on the impact of miR-129-2-3p on EC. Conclution: MiR-129-2-3p is a cancer repressor in EC cells, and it could target DNMT3B, thus hampering progression of EC cells.

This study tended to clarify the role of miR-126 in non-small cell lung cancer (NSCLC) cell biological behaviors in vitro, containing cell proliferation, migration, invasion, and apoptosis. miRNA expression microarray related to NSCLC was accessed from gene expression omnibus (GEO) database and subjected to differential analysis using the "limma" package. Real-time quantitative PCR was conducted to assess the expression of miR-126 in NSCLC cell lines.wIn vitro experiments including 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-Htetrazolium bromide (MTT), wound healing assay, Transwell, and flow cytometry assay were used for evaluating the effect of miR-126 on cell proliferation, migration, invasion, and apoptosis. Additionally, target mRNA for miR-126 was predicted and further validated by bioinformatics analysis and dualluciferase reporter assay, respectively. It suggested that miR-126 was significantly down-regulated in NSCLS based on the expression microarray, and similar expression trend was exhibited in cancer cell lines. In the meantime, overexpression of miR-126 was found to result in inhibition of cell proliferation, migration, and invasion while promotion of cell apoptosis, with reductions in protein expression of AKT2 and phosphorylated HK2 (p-HK2) as well. AKT2, identified to be a direct target of miR-126 in NSCLC as judged by dualluciferase reporter assay. Additionally, overexpression of AKT2 was observed to have the ability of elevating p-HK2 protein expression and reversing the effect of miR-126 on NSCLC cell proliferation, migration, and invasion. Given the above findings, we can see that miR-126 exerts its role in NSCLC cell proliferation, migration, invasion, and apoptosis with the aid of AKT2/HK2 axis.