Abstract

Objective Knockdown the Cyclin G1 in the A549 cell of lung cancer, to explore its effects on the proliferation and apoptosis of the A549 cell. Methods Cyclin G1 siRNA was transfected into A549 cells by using liposome transfection method, the expression levels of Cyclin G1 mRNA were detected by reverse transcriptase-polymerase chain reaction (RT-PCR), and the expression levels of β-catenin, c-Myc and Cyclin G1 proteins in A549 cells were detected by Western blotting technique. Thiazole blue methyl thiazol tetrazolium (MTT) method was used to detect the proliferation of A549 cells after 48 h transfection, and the flow cytometry detected changes in cell cycle and apoptosis rate. Results The absorbance value (A) and the expression levels of Cyclin G1 mRNA and β-catenin, c-Myc and Cyclin G1 proteins in A549 of the interference group were significantly lower than those of the control group (t=14.250, P=0.000, t=10.739, P=0.000). Compared with the control group, the proportion of cells of interference group after 48 h transfection in G0/G1 phaseand apoptosis ratesignificantly increased, proportion of cells in S phaseand G2/M phase significantly decreased, and the differences were statistically significant (t=5.074, P=0.007; t=4.634, P=0.010; t=3.099, P=0.000). Conclusion Knockdown Cyclin G1 gene can inhibit lung cancer cell proliferation and induce its apoptosis, the mechanism may be related to block the cell cycle in G0/G1 phase and cut β-catenin, c-Myc proteins in Wnt signaling pathways. Key words: Lung cancer; Cyclin G1; Cell proliferation; Cell apoptosis

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.