miR‑30a‑3p suppresses the proliferation and migration of lung adenocarcinoma cells by downregulating CNPY2

Lung cancer is a leading cause of cancer‑related morbidity and mortality worldwide. Although there are currently various therapeutic strategies including surgery, chemotherapy and radiotherapy, lung cancer still results in high mortality with a 5‑year survival rate of less than 20%. The increasing need for new therapeutic targets and diagnostic/prognostic tools for lung cancer has promoted the demand for a better molecular and mechanistic understanding of its pathobiology. microRNA‑30a‑3p (miR‑30a‑3p) was recently recognized to be closely involved in the regulation of cancer cell invasion, migration and proliferation. However, the mechanistic role of miR‑30a‑3p in regulating the biological behavior of lung cancer, especially lung adenocarcinoma (LADC), is unknown. In the present study, we aimed to confirm the downregulation of miR‑30a‑3p in LADC tissues, and validate its functional impact on the pathogenesis of LADC via its molecular target, canopy fibroblast growth factor signaling regulator 2 (CNPY2), a known oncogene. Our data confirmed that CNPY2 was upregulated in LADC tissues, and the expression level of CNPY2 was correlated with the clinical outcomes of lung cancer patients. miR‑30a‑3p was confirmed as a key negative regulator of CNPY2 and reduced miR‑30a‑3p expression resulted in CNPY2 upregulation in LADC tissues. We then validated the functional outcome of miR‑30a‑3p in cancer pathobiology by the overexpression of miR‑30a‑3p in the LADC EKVX cell line. miR‑30a‑3p overexpression inhibited cancer cell proliferation, invasion and migration, by suppressing CNPY2 expression. In addition, miR‑30a‑3p inhibited epithelial‑mesenchymal transition, a key feature of LADC, via CNPY2 suppression. Taken together, these findings suggest that miR‑30a‑3p exerts a novel inhibitory role in the pathogenesis of LADC via CNPY2 downregulation, and the miR‑30a‑3p/CNPY2 pathway is a potential therapeutic target for human LADC.