Objective: To study the effects of Pim-3 on lung adenocarcinoma A549 cells. A549 cells were divided into an untreated group (without any treatment), a scramble siRNA group (transfected with control siRNA), and a Pim-3-deficient group (transfected with Pim-3 siRNA).
Methods: Pim-3-deficient cells are the experimental sample, whereas scramble siRNA and untreated cells are the corresponding negative controls. Western blotting was performed to detect the expression levels of Pim-3 protein, the phosphorylation of signal transducer and activator of transcription 3 (STAT3), and the expression levels of downstream target genes (p21, cyclin D1, Bcl-2, and Bax). Flow cytometry was performed to analyze cell cycle and apoptosis.
Results: In the Pim-3-deficient group, Pim-3 was downregulated, the STAT3 phosphorylation level decreased, the levels of cyclin D1 and Bcl-2 decreased, but the levels of p21 and Bax increased. Meanwhile, cell proliferation was significantly inhibited (P<0.05); specifically, the G0/G1-phase cell proportion increased, whereas the S-phase cell proportion decreased and the proportion of early apoptotic cells increased significantly (P<0.05).
Conclusion: The downregulation of Pim-3 was closely related to the activation status of the lung STAT3 signaling pathway, mediated cell proliferation inhibition and induced apoptosis.
Keywords: Lung cancer; Moloney murine leukemia virus; STAT3 signaling pathway; provirus-integrating site.
© 2019 by the Association of Clinical Scientists, Inc.