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Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy

ABSTRACT: VAT-EVs from normal or obese mice, serum EVs from normal or obese mice and KPC cells sorted from allografts of normal mouse VAT-EV- or obese mouse VAT-EV-treated mice

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Blood Plasma, Extracellular Exosome Assembly

DISEASE(S): Obesity

SUBMITTER: Claire Chow

LAB HEAD: Claire Chow

PROVIDER: PXD066100 | Pride | 2025-10-29

REPOSITORIES: Pride

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			Action	DRS
	YE012ELQB2.zip	Other
	YE012ELQB2_CD_S_1.zip	Other
	YE012ELQB2_CD_S_2.zip	Other
	YE012ELQB2_CD_S_3.zip	Other
	YE012ELQB2_HFD_S_1.zip	Other

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Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy

Project description:VAT-EVs from normal or obese mice, serum EVs from normal or obese mice and KPC cells sorted from allografts of normal mouse VAT-EV- or obese mouse VAT-EV-treated mice

2025-10-29 | PXD066273 | Pride

Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy

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Proteomics on mouse obese and non-obese visceral adipose tissue derived extracellular vesicles

Project description:Visceral adipose tissue (VAT) was harvested from wild-type mice fed high-fat diet to induce obesity or matched diet as non-obese controls. VAT was ex vivo cultured for 48 hrs and its conditioned media was collected. Extracellular vesicles were isolated from conditioned media by ultracentrifugation. The aim of the project was to characterize extracellular vesicle protein cargo from obese and non-obese VAT.

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A long-term high fat diet induces differential gene expression changes in spatially distinct adipose tissues.

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Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy [RNA-seq]

Project description:Obesity is correlated with multitype of cancer development, and pancreatic ductal adenocarcinoma (PDAC) in obese patients often shows dismal prognosis and resistance to immune checkpoint blockade (ICB) therapy. The molecular mechanism for these phenomena is largely unknown. Here we show that obese visceral adipose tissues (VAT) can talk to distant PDAC by delivering their extracellular vesicle (EV) carrying signal molecules. We reveal that PDAC cells can take in VAT-EVs to their lysosomes where EVs-delivered Cathepsin A (Ctsa) stabilize ribonuclease Rnaset2b to produce extra pseudouridines from RNA cleavage. Pseudouridines released from cancer cells activate mast cells which inhibit CD8+ T cell activity, forming an immunosuppressive tumor microenvironment which enhances cancer progression and resistance to ICB. We also demonstrate the harmful effects of VAT-EV CTSA-pseudouridine-mast cell axis for PDAC in obese patients. Animal experiments indicate that Ctsa knockdown effectively enhances the ICB efficacy on PDAC. Our study uncovers a mechanism connecting obesity and cancer which holds promise for developing new therapeutic strategy for obesity related cancers.

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Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy [scRNA-seq]

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Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy [ATAC-seq]

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Project description:The protein Tsg101 plays an integral role extracellular vesicle formation and secretion from cells. We developed a mouse model with Tsg101 knockdown (Tsg101dAd). Visceral adipose tissue (VAT) was harvested from Tsg101dAD and Tsg101flfl mice fed high-fat diet to induce obesity or matched diet as non-obese controls. VAT was ex vivo cultured for 48 hrs and its conditioned media was collected. Extracellular vesicles were isolated from conditioned media by ultracentrifugation. The aim of the project was to characterize extracellular vesicle protein cargo from obese and non-obese VAT.

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Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy.

Project description:Obesity is correlated with multitype of cancer development, and pancreatic ductal adenocarcinoma (PDAC) in obese patients shows dismal prognosis and resistance to immune checkpoint blockade (ICB) therapy. The molecular mechanism is largely unknown. Here we show that obese visceral adipose tissues (VAT) can communicate with distant PDAC by delivering extracellular vesicle (EV) carrying signal molecules. We reveal that PDAC cells can take in VAT-EVs to their lysosomes where EVs-delivered Cathepsin A (Ctsa) stabilize ribonuclease Rnaset2b to produce free pseudouridines from RNA cleavage. Pseudouridines further activate mast cells via mediating an increase in reactive oxygen species (ROS) generation, which leads to a decrease in the distribution of H3K27me3 at the gene promoter, ultimately inhibiting CD8+ T cell activity, forming an immunosuppressive tumor microenvironment which enhances cancer progression and ICB resistance. We also demonstrate harmful effects of VAT-EV CTSA-pseudouridine-mast cell axis for obesity-related PDAC. Animal experiments indicate that Ctsa knockdown effectively enhances ICB efficacy on PDAC. Our study uncovers a mechanism connecting obesity and cancer which holds promise for developing new therapeutic strategy for obesity-related cancers.

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