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Determining genomic localization of SIX1 in A673 cells with SIX1 depletion

ABSTRACT: Determining genomic localization of SIX1 in A673 cells with SIX1 depletion

PROVIDER: PRJNA889827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21879735_1.fastq.gz	Fastqsanger.gz
	SRR21879735_2.fastq.gz	Fastqsanger.gz
	SRR21879736_1.fastq.gz	Fastqsanger.gz
	SRR21879736_2.fastq.gz	Fastqsanger.gz
	SRR21879737_1.fastq.gz	Fastqsanger.gz

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Determining genomic localization of SIX1 in A673 cells with SIX1 depletion

Project description:Investigating genomic binding of SIX1 in A673 cells transduced with shSCR or one of two shSIX1 shRNAs to deplete SIX1.

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

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

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

Project description:Investigating genomic binding of SIX1 in EWS-502 cells transduced with shSCR or one of two shSIX1 shRNAs to deplete SIX1.

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Effect of shRNA-mediated knockdown of SIX1 in A673 cells in vitro

Project description:To investigate gene expression changes associated with SIX1 in the A673 cell line

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Effect of shRNA-mediated knockdown of SIX1 in A673 cells in vitro

Project description:Effect of shRNA-mediated knockdown of SIX1 in A673 cells in vitro

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Differentiation resistant HPV16-immortalized keratinocytes: Six1 transfected vs. Control.

Project description:The overexpression of Six1, a member of the Six family of homeodomain transcription factors, has been found in various human cancers, and is associated with tumor progression and metastasis. We previously determined that the expression of Six1 mRNA increased during in vitro progression of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes (HKc/HPV16) toward a differentiation-resistant (HKc/DR) phenotype. However, if Six1 promotes HPV16-mediated transformation or not remains unknown. HKc/DR were transfected with a Six1 or control vector and RNA isolated from these cells were used in an Agilent two-color gene expression profiling experiment. The goal was to determine the effects of Six1 on global gene expression. Two-condition experiment, Six1 vs. Control HKc/DR cells. Biological replicates: 4 Six1-transfected replicates and 4 control-transfected replicates.

2013-12-24 | E-GEOD-53589 | biostudies-arrayexpress

Ectomesenchymal Six1 controls mandibular skeleton formation [CUT&Tag]

Project description:Craniofacial development requires intricate cooperation of multiple transcription factors and signaling pathways. Six1 is a critical transcription factor regulating craniofacial development. However, the exact function of Six1 during craniofacial development remains elusive. In this study, we investigated the function of Six1 in mandible development using a Six1 knockout mouse model (Six1-/-) and a cranial neural crest-specific, Six1 conditional knockout mouse model (Six1f/f; Wnt1-Cre). The Six1-/- mice exhibited multiple craniofacial deformities, including severe microsomia, high-arched palate, and uvula deformity. Importantly, the Six1f/f; Wnt1-Cre mice recapitulate the microsomia phenotype of Six1-/- mice, thus demonstrating that the expression of Six1 in ectomesenchyme is critical for mandible development. We further showed that the knockout of Six1 led to abnormal expression of osteogenic genes within the mandible. Moreover, the knockdown of Six1 in C3H10 T1/2 cells reduced their osteogenic capacity in vitro. Using RNA-seq, we showed that both the loss of Six1 in the E18.5 mandible and the Six1 knockdown in C3H10 T1/2 led to the dysregulation of genes involved in embryonal skeletal development. In particular, we showed that Six1 binds to the promoter of Bmp4, Fat4, Fgf18, and Fgfr2, and promotes their transcription. Collectively, our results suggest that Six1 plays a critical role in the regulation of mandibular skeleton formation during mouse embryogenesis.

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Ectomesenchymal Six1 controls mandibular skeleton formation [RNA-seq]

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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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