Abstract

Objective To observe the effect of over-expression of microRNA (miRNA, miR)-637 on the biological behaviors of thyroid cancer cell line TPC-1. Methods The over-expressed miR-637 plasmids (experimental group) and blank plasmid (negative control group) were transferred into TPC-1 cells respectively by lentivirus transfection. Cell proliferation was observed by cell counting kit-8 (CCK-8), cell apoptosis rate and cycle distribution were analyzed by flow cytometry, and scratch test and Transwell invasion test were used to evaluate the cell proliferation, cell migration and invasiveness. Results The growth curve of TPC-1 cells in the experimental group was relatively slow, and the cell growth rate was significantly lower than that in the negative control group (t=5.840, P=0.028). As compared with the negative control group [(12.50±1.71)%, the apoptosis rate of TPC-1 cells in the experimental group [(20.75±0.93)%] was significantly increased (t=19.674, P=0.003). The ratio of cell apoptosis was significantly higher in the experimental group than that in the negative control group. As compared with the experimental group, the percentage of cells in S phase was decreased to 23.35% after 48 h and that in G2/M phase decreased to 17.58%. Scratch test and Transwell invasion test showed that the number of migrating cells in the experimental group decreased significantly as compared with the negative control group (t=-26.186, P=0.001). Conclusion The over-expression of miR-637 can reduce the proliferation, apoptosis, migration and invasion of TPC-1 cells. Key words: Thyroid cancer; MicroRNA-637; Proliferation; Apoptosis; Migration; Invasion

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.