Effect of CLDN1 mAb on primary patient derived liver organoids
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851416 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19768573.fastq.gz | Fastqsanger.gz | |||
| SRR19768574.fastq.gz | Fastqsanger.gz | |||
| SRR19768575.fastq.gz | Fastqsanger.gz | |||
| SRR19768576.fastq.gz | Fastqsanger.gz | |||
| SRR19768577.fastq.gz | Fastqsanger.gz |
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Project description:Organoids were established from non-tumorous cirrhotic liver tissue and treated with CLDN1 mAb or Control mAb for 4 days. Organoids were harvested and mRNA was extracted. RNAsequencing was performed for comparative gene expression profiling.
2024-03-12 | GSE206581 | GEO
Project description:Cholangiocarcinoma (CCA) is an adenocarcinoma of the hepatobiliary system showing an alarming rise in incidence and mortality with unsatisfactory treatment options. Claudin-1 (CLDN1) is a transmembrane protein expressed in tight junctions and exposed on the cell surface in liver fibrosis and cancer. Using single cell RNA-sequencing (scRNA-Seq) and spatial transcriptomics of CCA patient tissues, we show that CLDN1 expression is highly upregulated in cancer cells and is associated with stemness and cell fate. Gain-of-function studies in CCA orthotopic in vivo mouse models showed decreased survival and enhanced tumor growth, unraveling a functional role of CLDN1 as an oncogenic driver. Targeting exposed CLDN1 using highly specific CLDN1 monoclonal antibodies (mAbs) robustly inhibited tumor growth across CCA CDX and PDX mouse models and patient-derived CCA organoids including tumors with medium or low CLDN1 expression. Moreover, antibody treatment markedly inhibited tumor cell migration, invasion, and extrahepatic metastasis. Mechanistically, targeting exposed CLDN1 on CCA tumors inhibited Notch1, and Hippo-YAP signaling, resulting in decreased cancer cell stemness, EMT and extracellular matrix remodeling. In conclusion, these results uncover CLDN1 as a previously undiscovered CCA driver and therapeutic target, paving the way for the clinical development of CLDN1 mAbs to improve the dismal outcome of patients with advanced CCA.
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Project description:Seven-week old male C57BL/6J mice received a single i.p. injection of DEN (100 mg/kg) and were subsequently fed with CDA-HFD after 3 weeks. After 6 weeks of diet, the mice were randomized in 2 groups, receiving weekly i.p. injections of 500 µg of either CLDN1 specific mAb or vehicle control for 16 weeks. RNA was extracted from non-tumorous liver tissue of 6 DEN-CDA-HFD mice treated with CLDN1 mAb, 6 DEN-CDA-HFD mice treated with vehicle Control as well as 5 C57BL/6J Control mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.
2024-03-12 | GSE174542 | GEO
Project description:Six-week old Fah−/−/Rag2−/−/Il2rg −/− (FRG) –NOD breeding mice were intravenously injected with 1.5 x 10^9 plaque forming units (pfu) of an adenoviral vector encoding the secreted form of the human urokinase-like plasminogen activator (Ad-uPA). Forty-eight hours later, 10^6 PHH were injected intrasplenically. Successfully transplanted mice were fed with CDA-HFD for 16 weeks and then treated with humanized CLDN1 specific mAb 500 µg or vehicle for additional 8 weeks. RNA was extracted from non-tumorous liver tissue of 4 NASH fibrosis mice treated with CLDN1 mAb, 3 vehicle Control treated NASH fibrosis mice as well as 3 humanized mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.
2024-03-12 | GSE174543 | GEO
Project description:Assessment of the effect of CLDN1 knockdown in cholangiocarcinoma patient-derived organoids
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Project description:Cholangiocarcinoma (CCA) is an adenocarcinoma of the hepatobiliary system showing an alarming rise in incidence and mortality with unsatisfactory treatment options. Claudin-1 (CLDN1) is a transmembrane protein expressed in tight junctions and exposed on the cell surface in liver fibrosis and cancer. Using single cell RNA-sequencing (scRNA-Seq) and spatial transcriptomics of CCA patient tissues, we show that CLDN1 expression is highly upregulated in cancer cells and is associated with stemness and cell fate. Gain-of-function studies in CCA orthotopic in vivo mouse models showed decreased survival and enhanced tumor growth, unraveling a functional role of CLDN1 as an oncogenic driver. Targeting exposed CLDN1 using highly specific CLDN1 monoclonal antibodies (mAbs) robustly inhibited tumor growth across CCA CDX and PDX mouse models and patient-derived CCA organoids including tumors with medium or low CLDN1 expression. Moreover, antibody treatment markedly inhibited tumor cell migration, invasion, and extrahepatic metastasis. Mechanistically, targeting exposed CLDN1 on CCA tumors inhibited Notch1 and Hippo-YAP signaling, resulting in decreased cancer cell stemness, EMT and extracellular matrix remodeling. In conclusion, these results uncover CLDN1 as a previously undiscovered CCA driver and therapeutic target, paving the way for the clinical development of CLDN1 mAbs to improve the dismal outcome of patients with advanced CCA.
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Project description:Cholangiocarcinoma (CCA) is an adenocarcinoma of the hepatobiliary system showing an alarming rise in incidence and mortality with unsatisfactory treatment options. Claudin-1 (CLDN1) is a transmembrane protein expressed in tight junctions and exposed on the cell surface in liver fibrosis and cancer. Using single cell RNA-sequencing (scRNA-Seq) and spatial transcriptomics of CCA patient tissues, we show that CLDN1 expression is highly upregulated in cancer cells and is associated with stemness and cell fate. Gain-of-function studies in CCA orthotopic in vivo mouse models showed decreased survival and enhanced tumor growth, unraveling a functional role of CLDN1 as an oncogenic driver. Targeting exposed CLDN1 using highly specific CLDN1 monoclonal antibodies (mAbs) robustly inhibited tumor growth across CCA CDX and PDX mouse models and patient-derived CCA organoids including tumors with medium or low CLDN1 expression. Moreover, antibody treatment markedly inhibited tumor cell migration, invasion, and extrahepatic metastasis. Mechanistically, targeting exposed CLDN1 on CCA tumors inhibited Notch1 and Hippo-YAP signaling, resulting in decreased cancer cell stemness, EMT and extracellular matrix remodeling. In conclusion, these results uncover CLDN1 as a previously undiscovered CCA driver and therapeutic target, paving the way for the clinical development of CLDN1 mAbs to improve the dismal outcome of patients with advanced CCA.
2026-06-08 | GSE312708 | GEO
Project description:Genome-wide RNAseq of liver tissue derived from DEN-CDA-HFD mice treated with CLDN1 mAb or vehicle Control
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Project description:Cholangiocarcinoma (CCA) is an adenocarcinoma of the hepatobiliary system showing an alarming rise in incidence and mortality with unsatisfactory treatment options. Claudin-1 (CLDN1) is a transmembrane protein expressed in tight junctions and exposed on the cell surface in liver fibrosis and cancer. Using single cell RNA-sequencing (scRNA-Seq) and spatial transcriptomics of CCA patient tissues, we show that CLDN1 expression is highly upregulated in cancer cells and is associated with stemness and cell fate. Gain-of-function studies in CCA orthotopic in vivo mouse models showed decreased survival and enhanced tumor growth, unraveling a functional role of CLDN1 as an oncogenic driver. Targeting exposed CLDN1 using highly specific CLDN1 monoclonal antibodies (mAbs) robustly inhibited tumor growth across CCA CDX and PDX mouse models and patient-derived CCA organoids including tumors with medium or low CLDN1 expression. Moreover, antibody treatment markedly inhibited tumor cell migration, invasion, and extrahepatic metastasis. Mechanistically, targeting exposed CLDN1 on CCA tumors inhibited Notch1, FAK/SRC, and Hippo-YAP signaling, resulting in decreased cancer cell stemness, EMT and extracellular matrix remodeling. In conclusion, these results uncover CLDN1 as a previously undiscovered CCA driver and therapeutic target, paving the way for the clinical development of CLDN1 mAbs to improve the dismal outcome of patients with advanced CCA.
2026-06-08 | GSE261997 | GEO
Project description:Cholangiocarcinoma (CCA) is an adenocarcinoma of the hepatobiliary system showing an alarming rise in incidence and mortality with unsatisfactory treatment options. Claudin-1 (CLDN1) is a transmembrane protein expressed in tight junctions and exposed on the cell surface in liver fibrosis and cancer. Using single cell RNA-sequencing (scRNA-Seq) and spatial transcriptomics of CCA patient tissues, we show that CLDN1 expression is highly upregulated in cancer cells and is associated with stemness and cell fate. Gain-of-function studies in CCA orthotopic in vivo mouse models showed decreased survival and enhanced tumor growth, unraveling a functional role of CLDN1 as an oncogenic driver. Targeting exposed CLDN1 using highly specific CLDN1 monoclonal antibodies (mAbs) robustly inhibited tumor growth across CCA CDX and PDX mouse models and patient-derived CCA organoids including tumors with medium or low CLDN1 expression. Moreover, antibody treatment markedly inhibited tumor cell migration, invasion, and extrahepatic metastasis. Mechanistically, targeting exposed CLDN1 on CCA tumors inhibited Notch1, FAK/SRC, and Hippo-YAP signaling, resulting in decreased cancer cell stemness, EMT and extracellular matrix remodeling. In conclusion, these results uncover CLDN1 as a previously undiscovered CCA driver and therapeutic target, paving the way for the clinical development of CLDN1 mAbs to improve the dismal outcome of patients with advanced CCA.
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