STK33 与自噬相互作用通过调控 mTOR/ULK1 信号通路促进肾细胞癌转移。
Interaction between STK33 and autophagy promoted renal cell carcinoma metastasis by regulating mTOR/ULK1 signaling pathway.
机构信息
Department of Pathology, The Affiliated Taian City Central Hospital of Qingdao University, No. 29, Longtan Road, Taishan District, Taian, 271000, China.
出版信息
Mol Biol Rep. 2023 Jun;50(6):5059-5067. doi: 10.1007/s11033-023-08396-3. Epub 2023 Apr 26.
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.
背景
STK33 在肾细胞癌（RCC）中的作用尚不清楚。本研究旨在探讨 STK33 与 RCC 中自噬之间的相互作用。
方法和结果
在 786-O 和 CAKI-1 细胞中敲低 STK33。然后进行 CCK8、克隆形成实验、划痕愈合实验和 Transwell 实验，以分析癌细胞的增殖、迁移和侵袭。此外，使用荧光测定法来确定自噬的激活，然后研究该过程中的潜在信号通路。在 STK33 敲低后，细胞系的增殖和迁移受到抑制，并且促进了肾癌细胞的凋亡。自噬荧光实验表明，在 STK33 敲低后，可以在细胞中看到绿色 LC3 蛋白荧光颗粒。Western blot 分析表明，在 STK33 敲低后，P62 和 p-mTOR 明显下调，Beclin1、LC3 和 p-ULK1 明显上调。
结论
STK33 通过激活 mTOR/ULK1 通路影响 RCC 细胞中的自噬。
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