Background: A vast majority of patients with NSCLC (non-small cell lung cancer) have lung adenocarcinoma (LA), and the survival rate of LA varies from 5% to 75% depending on the severity of this adenocarcinoma. PYCR1 (abnormal pyrroline-5-carboxylate reductase 1) gene and miR-328-3p have been found to be associated with cancer development. However, the underlying mechanism of interaction between miR-328-3p and PYCR1 in LA needs further investigation.
Methods: The expressions of miR-328-3p and PYCR1 in samples with LA were identified by RT-qPCR. Next, we investigated the targeting relationship between these two biological factors using luciferase assay. CCK-8, BrdU, transwell-migration, and flow cytometry assays were performed to detect cell viability, cell proliferation, cell migration and cell apoptosis in LA cells.
Results: We noticed that miR-328-3p expression was downregulated in LA samples. MiR-328-3p mimic restricted cell proliferation and cell migration, while it enhanced cell apoptosis. Furthermore, the overexpression of PYCR1 promoted the proliferation and migration of LA cells, but it repressed cell apoptosis. Moreover, PYCR1 directly interacted with miR-328-3p in the LA cells, and miR-328-3p restrained the expression of PYCR1, thus suppressing LA tumorigenesis.
Conclusion: In summary, our study revealed that miR-328-3p targeting to PYCR1 suppressed the malignancy of LA cells by impeding cell proliferation and migration, while effectively promoting cell apoptosis.
Keywords: Apoptosis; Lung adenocarcinoma; Migration; PYCR1; Proliferation; miR-328–3p.
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