Significance of SALL4 as a drug resistant factor in lung cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE56595 | GEO | 2014/04/30
SECONDARY ACCESSION(S): PRJNA244027
REPOSITORIES: GEO
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Project description:To examine the mechanism by which SALL4 regulates drug sensitivity, approximately 65,000 molecules on a microarray chip were analyzed using lung cancer cells transduced with a SALL4 vector (pCMV6-SALL4) or a control vector (pCMV6-Mock) . SALL4 mRNA and protein expression markedly increased after 24 hr of SALL4 vector transduction, unlike that in the cells transduced with the control vector; these cells were used for microarray analysis.
2014-04-30 | E-GEOD-56595 | biostudies-arrayexpress
Project description:To examine the mechanism by which SALL4 regulates drug sensitivity, approximately 65,000 molecules on a microarray chip were analyzed using lung cancer cells transduced with a SALL4 vector (pCMV6-SALL4) or a control vector (pCMV6-Mock) . SALL4 mRNA and protein expression markedly increased after 24 hr of SALL4 vector transduction, unlike that in the cells transduced with the control vector; these cells were used for microarray analysis.
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2020-04-01 | GSE129754 | GEO
Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder
2009-04-01 | GSE14219 | GEO
Project description:High confidence SALL4 targets were identified in mESCs by performing Cut&Run on SALL4 Flox/Flox and SALL4 -/- cells. We validated a commercially available antibody that specifically recognizes SALL4 protein.
2022-12-08 | GSE203303 | GEO
Project description:SALL4 is a nuclear factor central to the maintenance of stem cell pluripotency and is a key component in HCC, a malignancy with no effective treatment. In cancer cells, SALL4 associates with NuRD to silence tumor suppressor genes such as PTEN. Here, we design a potent therapeutic SALL4 peptide (FFW) capable of antagonizing the SALL4-NURD interaction using systematic truncation and amino acid substitution studies. To understand the pathways affected by the peptide treatment, we performed RNA sequencing on cells treated with different peptides. Furthermore, to identify SALL4 DNA binding targets, we have performed CRUD-ChIP sequencing with SALL4 and H2K27Ac antibodies on HCC cell line SNU398.
2018-07-05 | GSE112729 | GEO
Project description:Embryonic stem cells have potential utility in regenerative medicine due to their pluripotent characteristics. Sall4, a zinc-finger transcription factor, is expressed very early in embryonic development with Oct4 and Nanog, two well characterized pluripotency regulators. Sall4 plays an important role in governing the fate of stem cells through transcriptional regulation of both Oct4 and Nanog. Using chromatin immunoprecipitation coupled to microarray hybridization (ChIP on Chip), we have mapped global gene targets of Sall4 unveiling possible regulation of broad ES cell functions. Approximately 5,000 genes were identified that were bound by the Sall4 protein and many of these have major functions in developmental and regulatory pathways. Sall4 bound more than six times as many annotated genes within promoter regions as Oct4 and twice as many as Nanog. Immunoprecipitation revealed a heterotrimeric protein complex between Sall4, Oct4, and Nanog, consistent with binding site co-occupancies. Further, Sall4 bound many genes that are regulated in part by the chromatin-based epigenetic events mediated by polycomb-repressive complexes and bivalent domains. This suggests that Sall4 plays a central and diverse role in regulating stem cell pluripotency during early embryonic development that involves integration of transcriptional and epigenetic control processes. Keywords: ChIP-chip
2008-09-01 | GSE11305 | GEO
Project description:Sall genes are expressed early in development and in diversity of embryonic and adult structures. Sall4 plays a crucial role during the development of a number of systems. Mutations in the SALL4 gene have been linked to Okihiro/acro-renal-ocular syndrome, in which patients exhibit forearm malformations and eye movement deficits. Homozygote and heterozygote Sall4 cells from mouse blastocysts were collected and used to design a genetrap mouse mutant line. The homozygote Sall4 ES cells form mouse blastocyst were hybridizised versus TBV wildtype cells to detect changes in gene expression. Three biological samples of different passages of the same clone of NT1 and TBV were analyzed in 13 chip hybridizations; each sample was analyzed in 2-5 experimental replicates including dye swap experiments. Keywords: others
2006-08-02 | GSE4322 | GEO
Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder ES cells were cultured with or without mouse embryonic fibroblast (MEF) feeder cells in LIF-supplemented medium as described. To maintain the expression of Oct3/4, all ES cells were cultured in the presence of Blasticidin. Four samples were analyzed. GSM356329, GSM356330 : cultured in the absence of feeders GSM356331, GSM356332 : cultured on the feeders
2009-04-01 | E-GEOD-14219 | biostudies-arrayexpress
Project description:Embryonic stem cells have potential utility in regenerative medicine due to their pluripotent characteristics. Sall4, a zinc-finger transcription factor, is expressed very early in embryonic development with Oct4 and Nanog, two well characterized pluripotency regulators. Sall4 plays an important role in governing the fate of stem cells through transcriptional regulation of both Oct4 and Nanog. Using chromatin immunoprecipitation coupled to microarray hybridization (ChIP on Chip), we have mapped global gene targets of Sall4 unveiling possible regulation of broad ES cell functions. Approximately 5,000 genes were identified that were bound by the Sall4 protein and many of these have major functions in developmental and regulatory pathways. Sall4 bound more than six times as many annotated genes within promoter regions as Oct4 and twice as many as Nanog. Immunoprecipitation revealed a heterotrimeric protein complex between Sall4, Oct4, and Nanog, consistent with binding site co-occupancies. Further, Sall4 bound many genes that are regulated in part by the chromatin-based epigenetic events mediated by polycomb-repressive complexes and bivalent domains. This suggests that Sall4 plays a central and diverse role in regulating stem cell pluripotency during early embryonic development that involves integration of transcriptional and epigenetic control processes. Keywords: ChIP-chip We used ChIP-chip to map global promoter bound by Sall4, a zinc finger transcription factor. Growing evidence has suggested that Sall4 plays a vital role in ES cell pluripotency maintenance. Evidence for this includes its recent use as a marker for somatic cell reprogramming, in a genetic signature for ES cells, and evidence that Sall4 enhances reprogramming. These recent findings and two previously described interactions with Oct4 and Nanog strongly support the role of Sall4 in ES cells. This hypothesis was furthered here as we show that Sall4 plays important roles through transcriptional regulation of vital ES cell genes.
2008-09-01 | E-GEOD-11305 | biostudies-arrayexpress