Background: 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.
Methods and results: 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.
Conclusions: STK33 affected autophagy in RCC cells by activating mTOR/ ULK1pathway.
Keywords: Autophagy; Metastasis; Renal cancer; STK33; ULK1; mTOR.
© 2023. The Author(s), under exclusive licence to Springer Nature B.V.