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Interaction between STK33 and autophagy promoted renal cell carcinoma metastasis by regulating mTOR/ULK1 signaling

Xiaomei Li1, Min Lin2, Min Liu2

  • 1Department of Pathology, The Affiliated Taian City Central Hospital of Qingdao University, No. 29, Longtan Road, Taishan District, Taian, 271000, China. lxmcjcny@126.com.

Molecular Biology Reports
|April 26, 2023
PubMed
Abstract

Insights

Serine/threonine kinase 33 (STK33) impacts renal cell carcinoma (RCC) by influencing autophagy. STK33 knockdown inhibits cancer cell proliferation and migration via the mTOR/ULK1 pathway.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • The role of Serine/threonine kinase 33 (STK33) in renal cell carcinoma (RCC) is not well understood.
  • Investigating the interplay between STK33 and autophagy in RCC is crucial for understanding cancer progression.

Purpose of the Study:

  • To elucidate the functional role of STK33 in renal cell carcinoma.
  • To determine the relationship between STK33 and autophagy in RCC cells.

Main Methods:

  • STK33 was downregulated in RCC cell lines (786-O and CAKI-1).
  • Cell proliferation, migration, and invasion were assessed using CCK8, colony formation, wound healing, and Transwell assays.
  • Autophagy activation was analyzed via fluorescence microscopy and Western blotting, focusing on key proteins like LC3, Beclin1, p62, mTOR, and ULK1.

Main Results:

  • STK33 knockdown significantly inhibited proliferation and migration while promoting apoptosis in RCC cells.
  • Autophagy was activated following STK33 knockdown, evidenced by increased LC3 puncta.
  • Western blot analysis revealed decreased P62 and p-mTOR, and increased Beclin1, LC3, and p-ULK1 levels.

Conclusions:

  • STK33 plays a significant role in regulating autophagy in renal cell carcinoma.
  • The mTOR/ULK1 signaling pathway is implicated in STK33-mediated autophagy modulation in RCC.
Keywords:
AutophagyMetastasisRenal cancerSTK33ULK1mTOR

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