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Stem cell factor Sox2 regulates the tumorigenic potential in human gastric cancer cells

ABSTRACT: Gastric cancer is still one of the most common causes of cancer-related death worldwide, which is mainly attributable to late diagnosis and poor treatment options. Infection with H. pylori, different environmental factors and genetic alterations are known to influence the risk of developing gastric tumors. However, the molecular mechanisms involved in gastric carcinogenesis are still not fully understood, making it difficult to design targeted therapeutic approaches. Aberrant expression of the specific gastric differentiation marker Sox2 (sry-related HMG box 2) has been observed in stomach cancer. However, the role of Sox2 in gastric tumors has not been well established to date. To elucidate the role of Sox2 in gastric tumorigenesis, Sox2 transcriptional activity was blocked in AZ521 cells. Interestingly, inhibition of Sox2 reduced cell proliferation and migration, increased apoptosis and induced changes in cell cycle. Blocking of Sox2 also reduced the tumorigenic potential of AZ521 cells in vivo. In addition, correlation of Sox2 expression and proliferation was observed in a subset of human gastric tumours. Finally, target genes of Sox2 were for the first time identified by RNA microarray in gastric cancer cells. Taken together, the results presented here indicate that Sox2 controls several aspects related to gastric cancer development and progression by regulating the expression of members of important signalling pathways. These findings could provide new therapeutic options for a subset of gastric cancers exhibiting Sox2 deregulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42937 | GEO | 2013/12/31

SECONDARY ACCESSION(S): PRJNA183893

REPOSITORIES: GEO

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Stem cell factor Sox2 regulates the tumorigenic potential in human gastric cancer cells

Project description:Gastric cancer is still one of the most common causes of cancer-related death worldwide, which is mainly attributable to late diagnosis and poor treatment options. Infection with H. pylori, different environmental factors and genetic alterations are known to influence the risk of developing gastric tumors. However, the molecular mechanisms involved in gastric carcinogenesis are still not fully understood, making it difficult to design targeted therapeutic approaches. Aberrant expression of the specific gastric differentiation marker Sox2 (sry-related HMG box 2) has been observed in stomach cancer. However, the role of Sox2 in gastric tumors has not been well established to date. To elucidate the role of Sox2 in gastric tumorigenesis, Sox2 transcriptional activity was blocked in AZ521 cells. Interestingly, inhibition of Sox2 reduced cell proliferation and migration, increased apoptosis and induced changes in cell cycle. Blocking of Sox2 also reduced the tumorigenic potential of AZ521 cells in vivo. In addition, correlation of Sox2 expression and proliferation was observed in a subset of human gastric tumours. Finally, target genes of Sox2 were for the first time identified by RNA microarray in gastric cancer cells. Taken together, the results presented here indicate that Sox2 controls several aspects related to gastric cancer development and progression by regulating the expression of members of important signalling pathways. These findings could provide new therapeutic options for a subset of gastric cancers exhibiting Sox2 deregulation. Inducible dnSox2 in AZ521 cells, 4 timepoints with/without induction.

2013-12-31 | E-GEOD-42937 | biostudies-arrayexpress

ChIP-DSL H20K promoter array from human gastric cancer cells MKN28 with Sox2 overexpression

Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes. Transcription factor Sox2 promoter array in MKN28 cells with Sox2 overexpression.

2013-05-22 | E-GEOD-45427 | biostudies-arrayexpress

ChIP-DSL H20K promoter array from human gastric cancer cells MKN28 with Sox2 overexpression

2013-05-22 | GSE45427 | GEO

Gastric cancer custom mini-array

Project description:Gastric cancer (GC) is associated with high mortality rates and an unfavorable prognosis at advanced stages. In addition, there are no effective methods for diagnosing gastric cancer at an early stage or for predicting the outcome for the purpose of selecting patient-specific treatment options. Therefore, it is important to investigate new methods for GC diagnosis. We designed a custom microarray of gastric cancer. The customized microarray contained 1042 canceration and prognosis related genes identical to the probes on the Agilent microarray. DNA microarray profilling analysis was performed on gastric cancer tissues and premalignant tissues (20 samples per group).

2014-03-01 | E-MTAB-1881 | biostudies-arrayexpress

Sox2 suppresses gastric tumorigenesis in mice [CHIP-seq]

Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: Sox2 ChIP-enriched DNA and input DNA was isolated from gastric glands of adult antrum from Sox2 KO and Sox2 WT mice. DNA was purified and genomic libraries were prepared as described (Sulahian et al., 2014), using four micrograms of goat anti-SOX2 (AF2018, R&D). Libraries were sequenced (50 bp, single-end reads) on an Illumina Hi-Seq 2000 instrument. Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of wnt, intestinal and cancer related genes Examination of Sox2 targets in the stomachs of Sox2 WT and Sox2 KO mice.

2016-08-04 | E-GEOD-83965 | biostudies-arrayexpress

CHD7 and SOX2 Act in a Common Gene Regulatory Network During Mammalian Semicircular Canal and Cochlear Development (CUT&Tag)

Project description:Inner ear morphogenesis requires tightly regulated epigenetic and transcriptional control of gene expression. CHD7, an ATP-dependent chromodomain helicase DNA-binding protein, and SOX2, an SRY-related HMG box pioneer transcription factor, are known to contribute to vestibular and auditory system development, but their genetic interactions in the ear have not been explored. Here, we analyzed inner ear development and the transcriptional regulatory landscapes in mice with variable dosage of Chd7 and/or Sox2. We show that combined haploinsufficiency for Chd7 and Sox2 results in reduced otic cell proliferation, severe malformations of semicircular canals, and shortened cochlea with ectopic hair cells. Examination of mice with conditional, inducible Chd7 loss by Sox2CreER reveals a critical period (~E9.5) of susceptibility in the inner ear to combined Chd7 and Sox2 loss. Data from genome-wide RNA-sequencing and CUT&Tag studies in the otocyst show that CHD7 regulates Sox2 expression and acts early in a gene regulatory network to control expression of key otic patterning genes, including Pax2 and Otx2. CHD7 and SOX2 directly bind independently and cooperatively at transcription start sites and enhancers to regulate otic progenitor cell proliferation and function. Together, our findings reveal essential roles for Chd7 and Sox2 in the early inner ear and may be applicable for CHD7 and SOX2 related syndromic and other forms of hearing or balance disorders.

2024-03-01 | GSE239362 | GEO

CHD7 and SOX2 Act in a Common Gene Regulatory Network During Mammalian Semicircular Canal and Cochlear Development (RNA-Seq)

2024-03-01 | GSE239361 | GEO

Sox2 suppresses gastric tumorigenesis in mice [CHIP-seq]

2016-08-04 | GSE83965 | GEO

Sox2 suppresses gastric tumorigenesis in mice [RNA-seq]

Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: mRNA profiles of Sox2 WT and Sox2 KO gastric glands were generated by RNA-sequencing, in triplicate, using a Illumina HiSeq 2500 instrument, resulting in 36 million single-end 50bp reads per smaple. Sequencing reads were mapped to the mouse reference genome (mm10/GRCm38) using STAR (Dobin et al., 2013). Read counts over transcripts were calculated using HTSeq v.0.6.0 (Anders et al., 2015) based on a current Ensembl annotation file for mm10/GRCm38 (release 75). Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of cancer and intestinal related genes. mRNA profiles of stomachs from 10 week old Sox2 WT and Sox2 KO mice were generated by sequencing, in triplicate, using a Illumina HiSeq 2500.

2016-08-04 | E-GEOD-83964 | biostudies-arrayexpress

Genes regulated by SOX2 overexpression in gastric cancer cells

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2011-02-02 | GSE23589 | GEO

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