Streptococcus macedonicus strain:SGM CIP105683T
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA940176 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR24332397_subreads.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
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Project description:Streptococcus gallolyticus sp. gallolyticus (SGG) is a gut pathobiont involved in the development of colorectal cancer (CRC). To decipher SGG contribution in tumor initiation and/or acceleration respectively, a global transcriptome was performed in normal colonic cells (FHC) and in tumoral colonic cells (HT29). To identify SGG-specific alterations, we chose the phylogenetically closest relative, Streptococcus gallolyticus subsp. macedonicus (SGM) as control bacterium. We show that SGM, a bacterium generally considered as safe, did not induce any transcriptional changes on the two human colonic cells FHC and HT29. The transcriptional reprogramming induced by SGG in FHC and HT29 cells was significantly different, however most of the genes up- and down-regulated were associated with cancer disease. Top up-regulated genes related to cancer were: (i) IL-20, CLK1, SORBS2, ERG1, PIM1, SNORD3A for normal FHC cells and (ii) TSLP, BHLHA15, LAMP3, ZNF27B, KRT17, ATF3 for cancerous HT29 cells. SGG induces much stronger transcriptional changes in cancerous than in normal colonic cells (2090 vs genes 128). Gene set enrichment analysis reveals that SGG-induced strong ER- (endoplasmic reticulum) stress and UPR- (unfolded protein response) activation in colonic epithelial cells. Our results suggest that SGG induces a pro-tumoral shift in human colonic cells particularly in transformed cells potentially accelerating tumor development in the colon.
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Project description:Streptococcus gallolyticus subsp. gallolyticus (SGG), an opportunistic gram-positive pathogen responsible for septicemia and endocarditis in the elderly, is often associated with colon cancer (CRC). In this work, we investigated the oncogenic role of SGG strain UCN34 using the azoxymethane (AOM)-induced CRC model in vivo, organoids formation ex vivo and full proteomic and phosphoproteomic analysis from murine colons. To identify SGG-specific pathogenic traits, the choice of the control bacterium was important, and we selected the genetically closest and non-pathogenic relative of SGG named S. gallolyticus subsp. macedonicus (SGM). We showed that SGG UCN34 accelerates colon tumor development in the murine CRC model. To test SGG’s capacity to induce pre-cancerous transformation of the murine colonic epithelium, we grew ex vivo organoids which revealed unusual structures with compact morphology. To understand the molecular changes induced by SGG UCN34, we compared full proteome and phosphoproteome analysis of murine colon chronically colonized by SGG UCN34 or SGM. We found that 136 proteins and 583 phosphorylation sites were differentially regulated following colonization by SGG UCN34. Ingenuity Pathway Analysis (IPA) indicates a pro-tumoral shift induced specifically with SGG UCN34, as most proteins and phosphoproteins identified were associated with digestive cancer. Comprehensive analysis of the altered phosphoproteins using ROMA software revealed possible activation by SGG UCN34 of several cancer hallmark pathways, i.e. MAPK (ERK, JNK and p38), mTOR and integrin/ILK/actin signaling. Altogether, our results reveal for the first time that the oncogenic role of SGG UCN34 is associated with activation of multiple cancer-related signaling pathways which cannot be recapitulated in basic in vitro culture models.
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Project description:Streptococcus gallolyticus subsp. gallolyticus (SGG), an opportunistic gram-positive pathogen responsible for septicemia and endocarditis in the elderly, is often associated with colon cancer (CRC). In this work, we investigated the oncogenic role of SGG strain UCN34 using the azoxymethane (AOM)-induced CRC model in vivo, organoids formation ex vivo and full proteomic and phosphoproteomic analysis from murine colons. To identify SGG-specific pathogenic traits, the choice of the control bacterium was important, and we selected the genetically closest and non-pathogenic relative of SGG named S. gallolyticus subsp. macedonicus (SGM). We showed that SGG UCN34 accelerates colon tumor development in the murine CRC model. To test SGG’s capacity to induce pre-cancerous transformation of the murine colonic epithelium, we grew ex vivo organoids which revealed unusual structures with compact morphology. To understand the molecular changes induced by SGG UCN34, we compared full proteome and phosphoproteome analysis of murine colon chronically colonized by SGG UCN34 or SGM. We found that 136 proteins and 583 phosphorylation sites were differentially regulated following colonization by SGG UCN34. Ingenuity Pathway Analysis (IPA) indicates a pro-tumoral shift induced specifically with SGG UCN34, as most proteins and phosphoproteins identified were associated with digestive cancer. Comprehensive analysis of the altered phosphoproteins using ROMA software revealed possible activation by SGG UCN34 of several cancer hallmark pathways, i.e. MAPK (ERK, JNK and p38), mTOR and integrin/ILK/actin signaling. Altogether, our results reveal for the first time that the oncogenic role of SGG UCN34 is associated with activation of multiple cancer-related signaling pathways which cannot be recapitulated in basic in vitro culture models.
2023-09-22 | PXD038267 | Pride
Project description:Streptococcus gallolyticus subsp. gallolyticus (SGG), an opportunistic gram-positive pathogen responsible for septicemia and endocarditis in the elderly, is often associated with colon cancer (CRC). In this work, we investigated the oncogenic role of SGG strain UCN34 using the azoxymethane (AOM)-induced CRC model in vivo, organoids formation ex vivo and full proteomic and phosphoproteomic analysis from murine colons. To identify SGG-specific pathogenic traits, the choice of the control bacterium was important, and we selected the genetically closest and non-pathogenic relative of SGG named S. gallolyticus subsp. macedonicus (SGM). We showed that SGG UCN34 accelerates colon tumor development in the murine CRC model. To test SGG’s capacity to induce pre-cancerous transformation of the murine colonic epithelium, we grew ex vivo organoids which revealed unusual structures with compact morphology. To understand the molecular changes induced by SGG UCN34, we compared full proteome and phosphoproteome analysis of murine colon chronically colonized by SGG UCN34 or SGM. We found that 136 proteins and 583 phosphorylation sites were differentially regulated following colonization by SGG UCN34. Ingenuity Pathway Analysis (IPA) indicates a pro-tumoral shift induced specifically with SGG UCN34, as most proteins and phosphoproteins identified were associated with digestive cancer. Comprehensive analysis of the altered phosphoproteins using ROMA software revealed possible activation by SGG UCN34 of several cancer hallmark pathways, i.e. MAPK (ERK, JNK and p38), mTOR and integrin/ILK/actin signaling. Altogether, our results reveal for the first time that the oncogenic role of SGG UCN34 is associated with activation of multiple cancer-related signaling pathways which cannot be recapitulated in basic in vitro culture models.
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