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

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 L

SUBMITTER: Wang L 

PROVIDER: S-EPMC7248661 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature