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

ABSTRACT: To investigate gene expression changes associated with SIX1 in the EWS-502 cell line

ORGANISM(S): Homo sapiens

PROVIDER: GSE215354 | GEO | 2023/05/22

REPOSITORIES: GEO

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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.

2023-05-22 | GSE233118 | GEO

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

Project description: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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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

2023-05-22 | GSE215352 | GEO

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

| PRJNA889834 | ENA

Impact of EWS knockdown on LTBR mediated Gene Activation in human fibroblasts

Project description:LTβR signaling is crucial for immune development, homeostasis, and inflammation. To identify protein determinants that control the quality of LTβR function, we use a novel proteomics approach to identify EWS as a novel signaling component of this pathway. LTβR signaling protein, TRAF3, controls the protein binding activity of EWS via formation of mutually exclusive protein-protein interactions. With transcriptomics and knockdown experiments we identify several pro-inflammatory genes with induction kinetics that are controlled by EWS during LTβR signaling. Given the link between gene induction responsiveness and mRNA decay, we show EWS controls the decay of these transcripts.

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Synechococcus sp. CCFWC 502 isolate:CCFWC 502

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Homeoprotein SIX1 compromises anti-tumor immunity through TGF-β-mediated regulation of collagens

Project description:Purpose: The tumor microenvironment (TME), such as non-immune-infiltrated “cold” tumors, has been associated with immune suppression. However, the complex mechanisms regulating tumor immunogenicity have not been clearly elucidated. In this study, we investigated whether Transcription factor sine oculis homeobox 1 (SIX1) expression in the cancer cells regulated anti-tumor immunity by reshaping TME. Methods: The expression of SIX1 in human tumor tissues was analyzed based on TCGA data. Six1 knockout murine cell lines were generated to analyze the SIX1-associated tumor progression and anti-tumor immune response in tumor xenograft models. Immune cells and cytokines in TME were quantified by immunofluorescence, flow cytometry, quantitative reverse transcription-PCR, and ELISPOT assay. SIX1-associated differentially expressed genes were investigated in cancer cells and tissues with RNA-Seq. At the end, Correlation of SIX1 with TGFBR2 expression was assessed by Western blot and Dual-luciferase reporter assay. Results:SIX1 was highly upregulated in human tumor tissues, while rarely expressed in matched normal tissues. Deletion of the Six1 in cancer cells inhibited tumor growth, depending on adaptive immunity. Moreover, Six1 deficiency significantly enhanced CD8+ T cells infiltration, leading to eradication of poorly immunogenic tumors and maintaining a long-term protection from tumor re-challenge. Mechanistically, SIX1 as a transcription factor upregulated TGFBR2 expression, which induced collagen genes expression via the Smad2/3 phosphorylation, increased collagens deposition in TME and hampered CD8+ T cells infiltration. Conclusions: Six1 deletion in cancer cells improved tumor immunogenicity, leading to tumor destruction by enhancing anti-tumor immune responses. Our observations uncovered a crucial role of SIX1 on remodulating tumor immunogenicity and demonstrated a proof of concept for targeting SIX1 in cancer immunotherapy.

2021-09-09 | GSE183580 | GEO

Determining genomic localization of SIX1 in A673 cells with SIX1 depletion

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2023-05-22 | GSE215350 | GEO

Differential gene expression in GBS6 cells after EWS-POU5F1 knockdown

Project description:Our objective is to clarify the function of EWS-POU5F1 chimera. Specifially, GBS6 cells were established from an undifferentiated bone sarcoma carrying translocation t(6;22)(p21;q12). The translocation resulted in a gene fusion between EWS and POU5F1. Gene expression analysis of t(6;22) undifferentiated sarcoma cell line GBS6 transfected with POU5F1 specific siRNA to investigate the function of EWS-POU5F1. Knockdown of EWS-POU5F1 using POU5F1 specific siRNAs. 3 control and 6 experimental replicates representing the same experiment repeated 3 times (1st, 2nd, 3rd).

2009-05-31 | E-GEOD-12320 | biostudies-arrayexpress

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