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RNA-seq of KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs

ABSTRACT: RNA-seq of KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs

PROVIDER: PRJNA547719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9214220_1.fastq.gz	Fastqsanger.gz
	SRR9214220_2.fastq.gz	Fastqsanger.gz
	SRR9214221_1.fastq.gz	Fastqsanger.gz
	SRR9214221_2.fastq.gz	Fastqsanger.gz
	SRR9214222_1.fastq.gz	Fastqsanger.gz

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RNA-seq of KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs

Project description:We examined gene expression level in KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs to study the mechanism underlying the tumor suppressive effect of ARID1A and USP11.

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RNA-seq of A431 cells expressing control or ARID1A-targeting shRNAs

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YM155 treated KYSE410

Project description:We used microarrays to detail the gene expression profiles of KYSE410 cell line to identify distinct up and down-regulated genes during treatment with cisplatin. KYSE410 cell line were treated with 20 nM YM155 for 6 hrs and selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to gene expression profiles of KYSE 410 cell line treated with cisplatin.

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YM155 treated KYSE410

Project description:We used microarrays to detail the gene expression profiles of KYSE410 cell line to identify distinct up and down-regulated genes during treatment with cisplatin.

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gene expression of KYSE410 cells with control or treatment of 50 ng/mL CCL22

Project description:KYSE410 cells were treated with 50 ng/mL CCL22, and KYSE410 cells were collected for gene expression analysis using Agilent SurePrint G3 Human Gene Expression v3 (8×60K) Microarray. Investigation of the critical gene of KYSE410 cells treated by 50 ng/mL CCL22.

2025-05-05 | GSE202343 | GEO

USP11 promotes prostate cancer progression by upregulating AR and c-Myc activity [CUT&RUN]

Project description:Androgen receptor (AR) is a main driver for castration-resistant prostate cancer (CRPC). c-Myc is an oncogene underlying prostate tumorigenesis. Here we find that the deubiquitinase USP11 targets both AR and c-Myc in prostate cancer. USP11 expression was upregulated in metastatic prostate cancer and CRPC. USP11 knockdown significantly inhibited prostate cancer cell growth. Our RNA-seq studies revealed AR and c-Myc as the top transcription factors altered after USP11 knockdown. ChIP-seq analysis showed that either USP11 knockdown or replacement of endogenous USP11 with a catalytic-inactive USP11 mutant significantly decreased chromatin binding by AR and c-Myc. We find that USP11 employs two mechanisms to upregulate AR and c-Myc levels: namely, deubiquitination of AR and c-Myc proteins to increase their stability; deubiquitination of H2A-K119Ub, a repressive histone mark, on promoters of AR and c-Myc genes to increase their transcription. AR and c-Myc re-expression in USP11-knockdown prostate cancer cells partly rescued cell growth defects. Thus, our studies reveal a tumor-promoting role for USP11 in aggressive prostate cancer through upregulation of AR and c-Myc activities and support USP11 as a potential target against prostate cancer.

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USP11 promotes prostate cancer progression by upregulating AR and c-Myc activity [RNA-seq]

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Gene expression of KYSE410 cells with treatment of 10 uM FAK inhibitor (defactinib) for 4 hours and 24 hours

Project description:KYSE410 cells were treated with 10 uM defactinib for 4 hours and 24 hours,and KYSE410 cells were collected for gene expression analysis using Agilent SurePrint G3 Human Gene Expression v3 (8×60K) Microarray. Investigation of the critical gene of KYSE410 cells treated by defactinib.

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Project description:Since Usp11 encodes a DUB, we reasoned that Usp11 deficiency may lead to increased ubiquitination and destabilization of a protein that functions in neuronal differentiation and migration.To define the molecular mechanism of Usp11 deficiency on cortical development, we performed a label-free quantitative liquid chromatography-tandem Mass Spectrometry (LC-MS/MS) analysis to detect the protein expression profiles in E17.5 WT and Usp11 KO cortices in four biological repeats.

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