MicroRNA-196a promotes lung adenocarcinoma cell proliferation and invasion through targeting downregulation of lymphocyte cytosolic protein 2

Purpose Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide, yet the role of microRNA-196a (miR-196a) in LUAD progression is not fully understood. This study aimed to investigate the oncogenic potential of miR-196a in LUAD malignancy and its regulatory relationship with lymphocyte cytosolic protein 2 (LCP2), a putative tumor suppressor in solid tumors. Methods Expression levels of miR-196a and LCP2 were analyzed in LUAD tissues and paired adjacent non-tumor tissues using Reverse transcription-quantitative polymerase chain reaction (RT-qPCR). LUAD cell lines (NCI-H1299) and normal lung epithelial cells (BEAS-2B) were used for in vitro validation. Dual-luciferase reporter assays confirmed that miR-196a targets the 3’-Untranslated Region of LCP2. Functional assays (CCK-8 and Transwell assays) evaluated the effects of miR-196a mimics or inhibitors on proliferation, migration, and invasion. LCP2 expression was assessed at mRNA and protein levels by RT-qPCR and immunoblotting. Results Results revealed significant upregulation of miR-196a in LUAD tissues and cell lines, while LCP2 expression was markedly reduced. Dual-luciferase assays demonstrated that miR-196a overexpression significantly enhanced LUAD cell proliferation, migration, and invasion, while miR-196a inhibition attenuated these malignant phenotypes. Conclusion Mechanistically, the study identified miR-196a as a driver of LUAD malignancy through direct repression of LCP2, highlighting the miR-196a/LCP2 regulatory axis as a therapeutic target for precision intervention.