SALL4 Crud ChIP sequencing-WT and RNA-seq of SNU398 cells treated with therapeutic SALL4 peptides
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA448843 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6944460_1.fastq.gz | Fastqsanger.gz | |||
| SRR6944460_2.fastq.gz | Fastqsanger.gz | |||
| SRR6944461_1.fastq.gz | Fastqsanger.gz | |||
| SRR6944461_2.fastq.gz | Fastqsanger.gz | |||
| SRR6944462.fastq.gz | Fastqsanger.gz |
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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.
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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
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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.
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Project description:Bioactive peptides are promising agents for therapeutic applications, however their small size results in poor stability, low bioavailability and rapid renal clearance, so its widespread use is limited. To address these issues, fusing or conjugating peptides to suitable molecular scaffolds is required. In this study, human serum albumin (HSA) is used as a delivery carrier for human β-defensin-2 peptides (HBD2) in the production of HSA-delivered defensin complex (ADDC) to facilitate its cellular uptake and transport to intracellular targets. Conjugation can improve the stability of HBD2, while extend the circulation time and promote its accumulation within tumor, thereby improving the therapeutic efficacy. Herein, ADDC provides a protective structure against the harsh external environment and serves as a passive tumor-targeted system. Our data showed that the combination of ADDC with clinically relevant drugs, such as Doxorubicin, Gemcitabine, Cisplatin, and Cetuximab can significantly increase the cytotoxicity of ADDC on human pancreatic cancer cells. The results of bioinformatics analysis also revealed that ADDC may affect the metabolic processes, gene transcription and apoptosis of pancreatic cancer cells. Collectively, ADDC exhibited specific tumor targeting capabilities, low systemic toxicity, and enhanced antitumor efficacy in a mouse model of pancreatic cancer.
2020-12-23 | GSE149557 | GEO
Project description:The overall survival of lung cancer patients remains dismal despite the availability of targeted therapies. Oncofetal protein SALL4 is a novel cancer target. We herein report that SALL4 was aberrantly expressed in a subset of lung cancer patients with poor survival. SALL4 silencing by RNA interference or SALL4 peptide inhibitor treatment led to impaired lung cancer cell growth. Expression profiling on SALL4-knockdown cells demonstrated that both the EGFR and IGF1R signaling pathways were affected. Further studies revealed that SALL4 suppresses these pathways indirectly by repressing CBL-B. Connectivity Map analysis revealed HDAC inhibitor MS-275 as a potential drug in treating SALL4-expressing cancers and this was confirmed using 17 lung cancer cell lines. In summary, we report for the first time that MS-275 can target the novel SALL4/CBL-B pathway in lung cancer. This lays the foundation for future clinical studies to evaluate the therapeutic efficacy of MS-275 in SALL4-positive lung cancer patients.
2015-05-16 | GSE68959 | GEO
Project description:The zinc finger transcription factor SALL4 is highly expressed in embryonic stem cells, down-regulated in most adult tissues, but reactivated in many aggressive cancers. This unique expression pattern makes SALL4 an attractive target for designing therapeutic strategies. However, whether SALL4 binds DNA directly to regulate gene expression is unclear and many of its targets in cancer cells remain elusive. Here, through an unbiased screen of protein binding microarray (PBM) and Cleavage Under Targets and Release Using Nuclease (CUT&RUN) experiments, we identified and validated the DNA binding domain of SALL4 and its consensus binding sequence. Combined with RNA-seq analyses after SALL4 knockdown, we discovered hundreds of new SALL4 target genes that it directly regulates in aggressive liver cancer cells, including genes encoding a family of Histone 3 Lysine 9-specific Demethylases (KDMs). Taken together, these results elucidated the mechanism of SALL4 DNA binding and revealed novel pathways and molecules to target in SALL4-dependent tumors.
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Project description:The overall survival of lung cancer patients remains dismal despite the availability of targeted therapies. Oncofetal protein SALL4 is a novel cancer target. We herein report that SALL4 was aberrantly expressed in a subset of lung cancer patients with poor survival. SALL4 silencing by RNA interference or SALL4 peptide inhibitor treatment led to impaired lung cancer cell growth. Expression profiling on SALL4-knockdown cells demonstrated that both the EGFR and IGF1R signaling pathways were affected. Further studies revealed that SALL4 suppresses these pathways indirectly by repressing CBL-B. Connectivity Map analysis revealed HDAC inhibitor MS-275 as a potential drug in treating SALL4-expressing cancers and this was confirmed using 17 lung cancer cell lines. In summary, we report for the first time that MS-275 can target the novel SALL4/CBL-B pathway in lung cancer. This lays the foundation for future clinical studies to evaluate the therapeutic efficacy of MS-275 in SALL4-positive lung cancer patients. Cells from human lung carcinoma cell line H661 with wildtype scrambled controls or Sall4 knockdown were used for RNA extraction and hybridization on Affymetrix microarrays.
2015-05-16 | E-GEOD-68959 | biostudies-arrayexpress
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
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