Abstract
The roles of STK33 in renal cell carcinoma (RCC) remain unclear. This study was designed to investigate the interaction between STK33 and the autophagy in the RCC. STK33 was knocked down in 786-O and CAKI-1 cells. Then CCK8, clony formation assay, wound healing assay and Transwell assay were performed to analyze the proliferation, migration and invasion of the cancer cells. In addition, the activation of autophagy was determined using fluorescence, followed by investigating the potential signaling pathways in this process. After STK33 knockdown, the proliferation and migration of cell lines were inhibited, and the apoptosis of renal cancer cells was promoted. Autophagy fluorescence experiment showed that after STK33 knockdown, green LC3 protein fluorescence particles could be seen in the cells. Western blot analysis showed that after STK33 knockdown, there was significant down-regulation in P62 and p-mTOR, as well as significant up-regulation of Beclin1, LC3 and p-ULK1. STK33 affected autophagy in RCC cells by activating mTOR/ ULK1pathway.
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 callDisclaimer: 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.
