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SPOP promotes ubiquitination and degradation of LATS1 to enhance kidney cancer progression. | LitMetric

SPOP promotes ubiquitination and degradation of LATS1 to enhance kidney cancer progression.

EBioMedicine

Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China. Electronic address:

Published: June 2020

AI Article Synopsis

  • SPOP acts as an oncoprotein in kidney cancer by promoting tumor growth through the degradation of key regulatory proteins involved in cell proliferation and apoptosis.
  • The study utilized various methods including Co-IP, RT-PCR, and Western blotting to explore SPOP's role and discovered that it targets LATS1 for degradation, which is crucial in the Hippo tumor suppressor pathway.
  • By degrading LATS1, SPOP enhances cell proliferation and invasion in kidney cancer, indicating a new molecular mechanism behind its oncogenic function.

Article Abstract

Background: Emerging evidence has demonstrated that SPOP functions as an oncoprotein in kidney cancer to promote tumorigenesis by ubiquitination-mediated degradation of multiple regulators of cellular proliferation and apoptosis. However, the detailed molecular mechanism underlying the oncogenic role of SPOP in kidney tumorigenesis remains elusive.

Methods: Multiple approaches such as Co-IP, Transfection, RT-PCR, Western blotting, and animal studies were utilized to explore the role of SPOP in kidney cancer.

Findings: Here we identified LATS1, a critical component of the Hippo tumour suppressor pathway, as a novel ubiquitin substrate of SPOP. We found that LATS1 interacted with Cullin3, and depletion of Cullin 3 upregulated the abundance of LATS1 largely via prolonging LATS1 protein half-life. Mechanistically, SPOP specifically interacted with LATS1, and promoted the poly-ubiquitination and subsequent degradation of LATS1 in a degron-dependent manner. As such, over-expression of SPOP promoted cell proliferation partly through regulating cell cycle distribution in kidney cancer cells. Furthermore, SPOP also promoted kidney cancer cell invasion via degrading LATS1.

Interpretation: Our study provides evidence for a novel mechanism of SPOP in kidney cancer progression in part through promoting degradation of the LATS1 tumour suppressor.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7248661PMC
http://dx.doi.org/10.1016/j.ebiom.2020.102795DOI Listing

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