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Effect of shRNA-mediated knockdown of SIX1 in EWS-502 cells in vitro

ABSTRACT: Effect of shRNA-mediated knockdown of SIX1 in EWS-502 cells in vitro

PROVIDER: PRJNA889835 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21880054_1.fastq.gz	Fastqsanger.gz
	SRR21880054_2.fastq.gz	Fastqsanger.gz
	SRR21880055_1.fastq.gz	Fastqsanger.gz
	SRR21880055_2.fastq.gz	Fastqsanger.gz
	SRR21880056_1.fastq.gz	Fastqsanger.gz

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Effect of shRNA-mediated knockdown of SIX1 in EWS-502 cells in vitro

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Determining genomic localization of SIX1 in EWS-502 cells with SIX1 depletion

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Project description:Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed SIX1, MYOD1, and H3K27ac ChIPseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptional activity and myogenic transcription factor binding in fusion-negative Rhabdomyosarcoma.

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Expression data from SIX1 knocked-down HKc/DR cells

Project description:The homeodomain transcription factor SIX1 plays a critical role in embryogenesis, is not expressed in normal adult tissue, but is expressed in many malignancies, including cervical cancer. SIX1 drives the progression of HPV16-immortalized human keratinocytes (HKc/HPV16) toward malignancy: HKc/HPV16 express high levels of SIX1 mRNA and protein; overexpression of SIX1 in HKc/HPV16 produces pre-malignant, differentiation-resistant lines (HKc/DR); SIX1 overexpression in HKc/DR induces tumorigenicity. In this paper, we explore the consequences of inhibition of SIX1 expression in premalignant HKc/DR. Only partial inhibition of SIX1 expression could be obtained in HKc/DR by RNA interference. Decreased SIX1 expression (up to 80%) in HKc/DR resulted in slower proliferation, decreased HPV16-E6/E7 mRNA levels, and increased p53 protein levels. Gene expression changes induced in HKc/DR by anti-SIX1 shRNA were indicative of mesenchymal-epithelial transition (EMT) and changes in TGF-beta signaling. We conclude that HPV16-transformed cells depend on SIX1 for survival, continuous HPV16 E6/E7 gene expression and EMT.

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2022-02-07 | GSE173150 | GEO

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