miR-3615 suppresses proliferation and induces apoptosis in lung adenocarcinoma cells by targetting CALML4.

Abstract

Introduction and objective: MicroRNAs (miRNAs) are essential in the modulation of cellular activities. Studies suggest that miR-3615 may possess a tumour-suppressive function in lung adenocarcinoma (LUAD); however, its precise role and molecular mechanisms in LUAD progression remain incompletely understood. The aim of the study is to systematically investigate the biological functions and underlying mechanisms of miR-3615 in LUAD.

Material and methods: The expression of miR-3615 in LUAD cell lines was quantified by real-time quantitative PCR (RT-qPCR). Subsequently, its functional effects on proliferation, migration, invasion, and apoptosis were evaluated in A549 and H1299 cells using the CCK-8 assay, Transwell assay, and flow cytometry, respectively. Potential target genes of miR-3615 were predicted and functionally annotated using bioinformatics methods. The binding interaction of miR-3615 with the CALML4 gene was demonstrated via a dual-luciferase reporter assay.

Results: miR-3615 expression was notably downregulated in LUAD cell lines compared with normal cells. Overexpression of miR-3615 inhibited the proliferation, migration, and invasion capabilities of LUAD cells while promoting apoptosis. Integrated bioinformatics analysis involving target prediction and functional enrichment identified CALML4 as a key candidate target gene of miR-3615. CALML4 was confirmed as a direct target of miR-3615. The effects of miR-3615 mimic on LUAD cell proliferation, migration, invasion, and apoptosis were partly attenuated by CALML4 overexpression.

Conclusions: miR-3615 exerts its functional impact on LUAD cells by directly downregulating CALML4, thereby curbing proliferation, migration, and invasion and promoting apoptosis. The elucidated miR-3615/CALML4 axis advances the theoretical foundation for studying LUAD development.