Abstract
The purpose is to investigate the role of miR-28-5p in osteosarcoma (OS) development. The expressions of miR-28-5p and URGCP in OS tissues (n = 30) and cells (MG-63 and U2OS) were discovered by q-PCR assay. MiR-28-5p mimic, sh-URGCP, pcDNA3.1-URGCP, and their controls were transfected by lipofectamine ™2000. CCK8 and tunel experiments were processed for proliferation and apoptosis testing. Migration and invasion were monitored by transwell assay. Western blot was undertaken to show the levels of Bax and Bcl-2. The target between miR-28-5p and URGCP was confirmed via a luciferase reporter gene experiment. Finally, the rescue assay further verified the function of miR-28-5p and URGCP in OS cells. MiR-28-5p expressed lower (P < 0.001) in OS tissue and cells. MiR-28-5p mimics suppressed (P < 0.05) proliferation and migration ability, and it accelerated apoptosis of osteosarcoma cells. MiR-28-5p targeted and negatively regulated URGCP expression. Sh-URGCP suppressed (P < 0.01) proliferation and migration ability, while it improved apoptosis of OS cells. Overexpression of miR-28-5p obviously accelerated (P < 0.05) Bax expression, while it reduced (P < 0.05) the Bcl-2 level. Interestingly, pcDNA3.1-URGCP rescued the process. Up-regulated URGCP rescued the effects of miR-28-5p mimic in vitro. MiR-28-5p accelerates the proliferation and migration of osteosarcoma cells, and inhibits tumor cell apoptosis by suppressing URGCP expression, which could be regarded as a potential target for OS treatment.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
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.