USP39 promotes malignant proliferation and angiogenesis of renal cell carcinoma by inhibiting VEGF-A_165b alternative splicing via regulating SRSF1 and SRPK1.

ABSTRACT:

Background

The benefit of targeted therapy for renal cell carcinoma (RCC) is largely crippled by drug resistance. Rapid disease progression and poor prognosis occur in patients with drug resistance. New treatments demand prompt exploration for clinical therapies. Ubiquitin-specific peptidase 39 (USP39) serves as the pro-tumor factor in several previous studies of other malignant tumors. To investigate the function and mechanism of USP39 in promoting malignant proliferation and angiogenesis of RCC.

Methods

We applied ONCOMINE database to analyze the correlation between USP39 expression level and the clinical characteristics of RCC. USP39 knockdown or overexpression plasmids were transfected into 786-O and ACHN cells. The HUVEC received cell supernatants of 786-O and ACHN cell

SUBMITTER: Pan XW 

PROVIDER: S-EPMC8454004 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature