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Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance in Colorectal Cancer

ABSTRACT: Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance in Colorectal Cancer

PROVIDER: PRJNA573050 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10153024_1.fastq.gz	Fastqsanger.gz
	SRR10153024_2.fastq.gz	Fastqsanger.gz
	SRR10153025_1.fastq.gz	Fastqsanger.gz
	SRR10153025_2.fastq.gz	Fastqsanger.gz
	SRR10153026_1.fastq.gz	Fastqsanger.gz

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Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance

Project description:Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance

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Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance in Colorectal Cancer

Project description:The global up-regulation of histone acetylation modification after the activation of the TGF-β signaling pathway raised the possibility that the differential expression of specific histone acetyltransferases or histone deacetylases may involve in the modulation of TGF-β-associated chemoresistance in CRC. To test this hypothesis, high-throughput mRNA sequencing (RNA-Seq) was performed to compare the expression profile between SW480 cells treated with or without TGF-β1.

2022-09-01 | GSE137779 | GEO

Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance

Project description:Chip-seq analysis was performed to probe the epigenome related to TGF-β signaling pathway in colorectal cancer

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Hypoxic microenvironment activates GLI2 through synergistic action of TGF-β2 and HIF-1α to confer chemoresistance and poor clinical outcome in colorectal cancer [IlluminaExpr_2_CAF_SF_SD208]

Project description:Microenvironment has been suggested as an important factor contributing to how the colorectal cancer cells escape therapy, but the exact mechanism leading to chemoresistance remains elusive. Here, through modeling in vitro by cocultivation of patient-derived cancer associated fibroblasts (CAFs) with cancer stem cells (CSCs), we show that CAFs-secreted TGF-β2 is a key stromal factor that coordinates with hypoxia to promote CSC stemness and resistance to chemotherapy. GLI2, a key transcription factor of Hedgehog pathway, was identified as both necessary and sufficient in this process in which TGF-β and hypoxia-inducible factor (HIF-1α) synergize to directly induce GLI2 expression. Conversely, CSC-secreted TGF-β is also important to support the growth of CAFs but instead induce death of normal fibroblasts, suggesting a reciprocal mechanism to selectively support the CAF-CSC interaction. Small molecule inhibition of both TGF-β and GLI2 effectively reversed the chemoresistance. Finally, expression of TGFB2/HIF1A/GLI2 gene signature as a functional readout of this resistance pathway defines worse clinical outcomes and predicts patients relapse. Our observations uncover a key role of TGF-β/HIF-1α/GLI2 in microenvironment-mediated chemoresistance and reveal novel biomarker and targeting strategies to identify and treat the high risk CRC patients.

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SIK1 suppresses colorectal cancer metastasis and chemoresistance via the TGF-β signaling pathway.

Project description:In the present study, we investigated the role of salt-induced kinase 1 (SIK1), a serine/threonine kinase protein, in colorectal cancer (CRC). Despite the reported association of SIK1 with tumor malignancy suppression in various cancers, limited research has been conducted on its function in CRC. Our findings revealed that SIK1 expression was low in CRC cells. The results of a KEGG pathway analysis showed a strong association between SIK1 and the TGF-β signaling pathway. In addition, a coimmunoprecipitation assay validated the interaction between SIK1 and Smad7. Our data indicate that SIK1 inhibited the phosphorylation of Smad2, a critical molecule in the Smad-related TGF-β pathway, and downstream target genes of the TGF-β pathway. Furthermore, SIK1 was found to inhibit indicators of epithelial-mesenchymal transition (EMT) and reverse oxaliplatin resistance in CRC. Additionally, SIK1 reduced cell migration and invasion. Our results suggest that the inhibitory effect of SIK1 on the TGF-β pathway contributes to the suppression of metastasis and oxaliplatin chemoresistance in CRC. However, this effect was reversed by galunisertib (LY2157299). In conclusion, our findings provide novel insights into the role of SIK1 in the regulation of the TGF-β pathway in CRC, suggesting its potential as a therapeutic target for the treatment of CRC. Further studies are required to fully characterize the mechanism underlying these observations and to validate these findings in animal models.

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Genome wide identification of acetyl-CoA regulated loci

Project description:In order to identify regions of the genome that display quantitative changes in acetyl-CoA, we utilized an established “spike-in” normalization method that allows the quantitative comparison of histone modifications across cell populations using defined quantities of a reference epigenome. We found that some regions of the genome are more sensitive to changes in acetyl-CoA compared to others.

2018-12-20 | GSE109340 | GEO

Long Noncoding RNA TINCR-mediated Regulation of Acetyl-CoA Metabolism Promotes Nasopharyngeal Carcinoma Progression and Chemoresistance

Project description:Long Noncoding RNA TINCR-mediated Regulation of Acetyl-CoA Metabolism Promotes Nasopharyngeal Carcinoma Progression and Chemoresistance

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Project description:Emerging evidence indicates that metabolic enzymes perform moonlighting functions during tumor progression, including the modulation of chemoresistance. However, the underlying mechanisms of these functions remain elusive. In this study, utilizing a metabolic CRISPR-Cas9 knockout library screen, we observed that loss of Glutamate-cysteine ligase modifier subunit (GCLM), a rate-limiting enzyme in glutathione biosynthesis, noticeably heightens the sensitivity of colorectal cancer (CRC) cells to platinum-based chemotherapy. Mechanistically, we unveil a noncanonical mechanism through which nuclear GCLM competitively interacts with NF-kappa-B-repressing factor (NKRF), a known inhibitor of NF-κB signaling, to promote NF-κB activity and subsequently facilitate chemoresistance. In response to platinum drug treatment, P38 MAPK phosphorylates GCLM at T17, resulting in its recognition by importin a5 and subsequent nuclear translocation. Furthermore, elevated expression of nuclear GCLM correlates with unfavorable prognosis and poor benefit from standard chemotherapy. Overall, our work shed light on the essential nonmetabolic role and posttranslational regulatory mechanism of GCLM in enhancing NF-κB activity and subsequent chemoresistance.

2024-11-15 | PXD055376 | Pride

Global Stability Profling of Colorectal Cancer Chemoresistance

Project description:Almost half of the patients with advanced colorectal cancer (CRC) are resistant to oxaliplatin based therapy, the first line treatment for CRC. Therefore, predicting and understanding oxaliplatin resistance is important to improve CRC patient survival. Investigated here is the use of proteomic folding stability measurements to differentiate oxaliplatin resistant and sensitive CRCs using patient-derived CRC cell lines and patient-derived xenografts (PDXs). Three protein stability profiling techniques (including the Stability of Proteins from Rates of Oxidation (SPROX), the Thermal Protein Profiling (TPP), and Limited Proteolysis (LiP) approaches) were employed to identify differentially stabilized proteins in 6 patient-derived CRC cell lines with different oxaliplatin sensitivities and 8 CRC PDXs derived from 2 of the patient derived cell lines with different oxaliplatin sensitivity. A total of 23 proteins were found in at least 2 techniques to be differentially stabilized in both the cell line and PDX studies of oxaliplatin resistance. These 23 differentially stabilized proteins included 9 proteins that have been previously connected to cancer chemoresistance. Over-representation analysis (ORA) of all the differentially stabilized proteins identified here, revealed novel pathways related to oxaliplatin resistance. Compared to conventional protein expression level analyses, which were also performed on the cell lines and PDXs, the stability profiling techniques identified novel proteins and pathways and provided new insight on the molecular basis of oxaliplatin resistance. Our results suggest that protein stability profiling techniques are complementary to expression level analyses for identifying biomarkers and understanding molecular mechanisms associated with oxaliplatin chemoresistance in CRC and disease phenotypes in general.

2023-04-28 | PXD036298 | Pride

Long Noncoding RNA TINCR-mediated Regulation of Acetyl-CoA Metabolism Promotes Nasopharyngeal Carcinoma Progression and Chemoresistance

Project description:Our present study showed that lncRNA TINCR have impact on the ubiquitination-mediated degradation level of ACLY protein in nasopharyngeal carcinoma. Silencing of TINCR lead to downregulation of ACLY protein level. ACLY is a cytosolic homotetrameric enzyme catalyzing the ATP-dependent conversion of citrate and coenzyme A (CoA) to oxaloacetate and acetyl-CoA, a precursor for lipid biosynthesis, including cholesterol, free fatty acid and phospholipid. Meanwhile, the cellular acetyl-CoA pool is also required for acetylation reactions that modify proteins such as histone acetylation, including Histone H3 acetylation K27 (H3K27ac). To select the shared genes that were regulated by TINCR and were in response to acetyl-CoA alteration, we conducted RNA-seq in HONE-1 cells with or without TINCR or ACLY silencing, as well as H3K27ac Chromatin Immunoprecipitation sequencing (ChIP-seq) in HONE-1 cells with or without ACLY silencing. We also performed CLIP-seq in HONE-1 and SUNE-1 cells to validate the TINCR-ACLY interaction and identify the binding sites of TINCR with ACLY.

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