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Target BUB1 kinase as a therapeutic strategy for inhibiting STAT3 signal pathway in Bladder cancer

ABSTRACT: Target BUB1 kinase as a therapeutic strategy for inhibiting STAT3 signal pathway in Bladder cancer

PROVIDER: PRJNA534083 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8938070_1.fastq.gz	Fastqsanger.gz
	SRR8938070_2.fastq.gz	Fastqsanger.gz
	SRR8938071_1.fastq.gz	Fastqsanger.gz
	SRR8938071_2.fastq.gz	Fastqsanger.gz
	SRR8938072_1.fastq.gz	Fastqsanger.gz

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Target BUB1 kinase as a therapeutic strategy for inhibiting STAT3 signal pathway in Bladder cancer

Project description:The incidence for bladder urothelial carcinoma (UC), a common malignancy of the urinary tract, is about three times higher in men than in women. High expression of the mitotic kinase BUB1 is associated with a subset of human cancers, but how BUB1 drive Bladder tumorigenesis mechanism was unknown. Using a microarray approach, we identified BUB1 higher expression in BC. Moreover we found BUB1, a member of the kinase family as a STAT3 interactor and phosphorylated STAT3 at Ser727 in cell of bladder cancer. In vitro binding and kinase assays showed that BUB1 directly band STAT3 and phosphorylated STAT3. Furthermore, the BUB1/STAT3 complex promoted STAT3 target gene transcription. Depletion of BUB1 and expression of BUB1 kinase mutants abrogated target gene transcription, highlighting the essential function of the kinase activity in STAT3 target gene activation. Pharmacological inhibitors of BUB1 (2OH-BNPP1) was able to inhibit the growth of Bladder cancer cell xenograft. This kinase may present an attractive candidate for drug targeting in Bladder cancer.

2021-12-08 | GSE130145 | GEO

TRIM59 promotes gliomagenesis by inhibiting TC45 dephosphorylation of STAT3

Project description:Although the oncogenic signalings driven by amplification and mutations of EGF receptor (EGFR) gene play a major role in glioblastoma pathogenesis, the responsible downstream mechanisms remain less clear. Here we demonstrate that tripartite motif-containing protein 59 (TRIM59), acting as a new downstream effector of EGFR signaling, regulates STAT3 activation in glioblastoma. EGFR signaling leads to TRIM59 upregulation through SOX9 that results in enhancing TRIM59 interaction with STAT3 in nucleus, and inhibiting STAT3 association with TC45 (the nuclear form of T cell protein tyrosine phosphatase TC-PTP), thereby maintaining STAT3 phosphorylation and activation and promoting tumorigenesis. Silencing TRIM59 suppresses cell proliferation, migration, and orthotopic xenograft brain tumorigenesis of GBM cells. Moreover, evaluation of GBM patient samples reveals an association among EGFR activation, TRIM59 expression, STAT3 phosphorylation, and poor prognoses. Our study identifies TRIM59 as a new regulator of oncogenic EGFR-STAT3 signaling and a potential therapeutic target for GBM patients with EGFR activation.

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