ArticleMolecular biology reports2023
Interaction between STK33 and autophagy promoted renal cell carcinoma metastasis by regulating mTOR/ULK1 signaling pathway.
Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- ML281 Does Not Function as an STK33 Inhibitor but Modulates Proliferation and Differentiation of Keratinocytes Derived from Hypertrophic Scars.International journal of molecular sciences · 2026Article
- STK33 as the functional substrate of miR-454-3p for suppression and apoptosis in neuroblastoma.Molecules and cells · 2024Article
- Reversible male contraception by targeted inhibition of serine/threonine kinase 33.Science (New York, N.Y.) · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe 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
resultsSTK33 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.
conclusionsSTK33 affected autophagy in RCC cells by activating mTOR/ ULK1pathway.
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