High mobility group A1 (HMGA1) promotes esophageal squamous cell carcinoma progression by inhibiting STING-mediated anti-tumor immunity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1097547 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28592101_1.fastq.gz | Fastqsanger.gz | |||
| SRR28592101_2.fastq.gz | Fastqsanger.gz | |||
| SRR28592102_1.fastq.gz | Fastqsanger.gz | |||
| SRR28592102_2.fastq.gz | Fastqsanger.gz | |||
| SRR28592103_1.fastq.gz | Fastqsanger.gz |
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Project description:Esophageal squamous cell carcinoma (ESCC) is a common and aggressive cancer with limited responses to immunotherapy. High mobility group A1 (HMGA1), a chromatin remodeling protein, plays a key role in tumor progression, but its impact on anti-tumor immunity in ESCC remains unclear. Here we show that HMGA1 suppresses the stimulator of interferon genes (STING), inhibiting type I interferon secretion, downregulating interferon-stimulated genes, and impairing tumor-infiltrating lymphocyte (TIL) recruitment. HMGA1 inhibits STING transcription by competing with the coactivator CBP/p300 for binding to CREB. ESCCs from genetically modified mouse models with altered HMGA1 and STING expression exhibit varying TIL levels and sensitivity to STING agonists. Additionally, we design and synthesize a series of HMGA1 inhibitors, including a perylene-based nanoparticle, PDIC-DPC, which effectively inhibits HMGA1 and enhances TIL infiltration. Our findings identify HMGA1 as a critical immune checkpoint in ESCC and suggest that targeting HMGA1 could improve immunotherapy outcomes.
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Project description:Analysis of MDA-MB-231 breast cancer cells depleted for High Mobility Group A1 (HMGA1) using siRNA. HMGA1 is involved in invasion and metastasis in breast cancer cells. Results identify the specific transcriptional program induced by HMGA1 in highly metastatic breast cancer cells.
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Project description:Analysis of MDA-MB-231 breast cancer cells depleted for High Mobility Group A1 (HMGA1) using siRNA. HMGA1 is involved in invasion and metastasis in breast cancer cells. Results identify the specific transcriptional program induced by HMGA1 in highly metastatic breast cancer cells. MDA-MB-231 cells were transfected with HMGA1-specific siRNA or a control siRNA. Transfections were performed by using Lipofectamin RNAiMAX (Invitrogen) according to the manufacturer's procedure. Seventy-two hours after transfection, samples were processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each of the two conditions, for a total of 8 samples.
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Project description:Emerging evidence suggests that tumor cells metastasize by co-opting stem cell transcriptional networks, although the molecular underpinnings of this process are poorly understood. Here, we show for the first time that the high mobility group A1 (HMGA1) gene drives metastatic progression in triple negative breast cancer cells (MDA-MB-231) by reprogramming cancer cells to a stem-like state. We discovered an HMGA1 signature in triple negative breast cancer cells that is highly enriched in embryonic stem cells. Together, these findings indicate that HMGA1 is a master regulator of tumor progression in breast cancer by reprogramming cancer cells through stem cell transcriptional networks. Future studies are needed to determine how to target HMGA1 in therapy. HMGA1 was knocked-down in MDA-MB-231 cells using siRNA as we previously described (Tesfaye A 2007). RNA from three independent knockdown experiements along with 3 control populations were collected by Rneasy miniprep (Qiagen) and analyzed by Affymetrix Human Exon 1.0 ST platform.
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Project description:Emerging evidence suggests that tumor cells metastasize by co-opting stem cell transcriptional networks, although the molecular underpinnings of this process are poorly understood. Here, we show for the first time that the high mobility group A1 (HMGA1) gene drives metastatic progression in triple negative breast cancer cells (MDA-MB-231) by reprogramming cancer cells to a stem-like state. We discovered an HMGA1 signature in triple negative breast cancer cells that is highly enriched in embryonic stem cells. Together, these findings indicate that HMGA1 is a master regulator of tumor progression in breast cancer by reprogramming cancer cells through stem cell transcriptional networks. Future studies are needed to determine how to target HMGA1 in therapy.
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Project description:High Mobility Group A1 (HMGA1) is an architectural chromatin-binding protein that regulates gene expression in various biological contexts, including differentiation and cancer. While previous studies show that HMGA1 acts by binding specific gene promoters or by contributing to the enhanceosome, its global effect on transcription remains unclear. HMGA1 is also critical for the formation of senescence-associated heterochromatic foci (SAHF) in oncogene-induced senescence (OIS), a stable form of cell cycle arrest with a pro-inflammatory phenotype. This link between the two roles of HMGA1, gene regulation and chromatin organisation, has not been fully explained. Here, we used graph theory and data integration from high-throughput assays to investigate how HMGA1 binding impacts the chromatin interactions network. Our results demonstrate that HMGA1 profoundly remodels the global chromatin network during OIS and contributes to stronger compartmentalization. This remodelling goes beyond SAHF, leading to substantial gene repositioning and differential gene expression, highlighting a novel role for HMGA1 in altering chromatin environments. The HMGA1 effects of gene expression go beyond senescence and appear to be relevant in other contexts, such as lung cancer.
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Project description:High Mobility Group A1 (HMGA1) is an architectural chromatin-binding protein that regulates gene expression in various biological contexts, including differentiation and cancer. While previous studies show that HMGA1 acts by binding specific gene promoters or by contributing to the enhanceosome, its global effect on transcription remains unclear. HMGA1 is also critical for the formation of senescence-associated heterochromatic foci (SAHF) in oncogene-induced senescence (OIS), a stable form of cell cycle arrest with a pro-inflammatory phenotype. This link between the two roles of HMGA1, gene regulation and chromatin organisation, has not been fully explained. Here, we used graph theory and data integration from high-throughput assays to investigate how HMGA1 binding impacts the chromatin interactions network. Our results demonstrate that HMGA1 profoundly remodels the global chromatin network during OIS and contributes to stronger compartmentalization. This remodelling goes beyond SAHF, leading to substantial gene repositioning and differential gene expression, highlighting a novel role for HMGA1 in altering chromatin environments. The HMGA1 effects of gene expression go beyond senescence and appear to be relevant in other contexts, such as lung cancer.
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Project description:High Mobility Group A1 (HMGA1) is an architectural chromatin-binding protein that regulates gene expression in various biological contexts, including differentiation and cancer. While previous studies show that HMGA1 acts by binding specific gene promoters or by contributing to the enhanceosome, its global effect on transcription remains unclear. HMGA1 is also critical for the formation of senescence-associated heterochromatic foci (SAHF) in oncogene-induced senescence (OIS), a stable form of cell cycle arrest with a pro-inflammatory phenotype. This link between the two roles of HMGA1, gene regulation and chromatin organisation, has not been fully explained. Here, we used graph theory and data integration from high-throughput assays to investigate how HMGA1 binding impacts the chromatin interactions network. Our results demonstrate that HMGA1 profoundly remodels the global chromatin network during OIS and contributes to stronger compartmentalization. This remodelling goes beyond SAHF, leading to substantial gene repositioning and differential gene expression, highlighting a novel role for HMGA1 in altering chromatin environments. The HMGA1 effects of gene expression go beyond senescence and appear to be relevant in other contexts, such as lung cancer.
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Project description:High Mobility Group A1 (HMGA1) is an architectural chromatin-binding protein that regulates gene expression in various biological contexts, including differentiation and cancer. While previous studies show that HMGA1 acts by binding specific gene promoters or by contributing to the enhanceosome, its global effect on transcription remains unclear. HMGA1 is also critical for the formation of senescence-associated heterochromatic foci (SAHF) in oncogene-induced senescence (OIS), a stable form of cell cycle arrest with a pro-inflammatory phenotype. This link between the two roles of HMGA1, gene regulation and chromatin organisation, has not been fully explained. Here, we used graph theory and data integration from high-throughput assays to investigate how HMGA1 binding impacts the chromatin interactions network. Our results demonstrate that HMGA1 profoundly remodels the global chromatin network during OIS and contributes to stronger compartmentalization. This remodelling goes beyond SAHF, leading to substantial gene repositioning and differential gene expression, highlighting a novel role for HMGA1 in altering chromatin environments. The HMGA1 effects of gene expression go beyond senescence and appear to be relevant in other contexts, such as lung cancer.
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