Dataset Information

Secretome from human pancreatic ductal cells (HPDE)

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is characterised by an abundant desmoplastic reaction which includes an excess production of extracellular matrix. The proteins and extracellular matrix secreted by HPDE cells (H6c7), with and without expression of mutant KRas G12V, was analysed by LC-MSMS

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Pancreatic Ductal Carcinoma

SUBMITTER: Jon Humphries

LAB HEAD: Martin J Humphries

PROVIDER: PXD027823 | Pride | 2022-05-20

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20171206_JH_01.raw	Raw
	20171206_JH_01.raw__20171206_JH_01_plus_mods_.mzid.gz	Mzid
	20171206_JH_01.raw__20171206_JH_01_plus_mods_.mzid_20171206_JH_01.raw__20171206_JH_01_plus_mods_.MGF	Mzid
	20171206_JH_02.raw	Raw
	20171206_JH_02.raw__20171206_JH_02_plus_mods_.mzid.gz	Mzid

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Publications

Pancreatic ductal adenocarcinoma cells employ integrin α6β4 to form hemidesmosomes and regulate cell proliferation.

Humphries Jonathan D JD Zha Junzhe J Burns Jessica J Askari Janet A JA Below Christopher R CR Chastney Megan R MR Jones Matthew C MC Mironov Aleksandr A Knight David D O'Reilly Derek A DA Dunne Mark J MJ Garrod David R DR Jorgensen Claus C Humphries Martin J MJ

Matrix biology : journal of the International Society for Matrix Biology 20220409

Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis due to its aggressive progression, late detection and lack of druggable driver mutations, which often combine to result in unsuitability for surgical intervention. Together with activating mutations of the small GTPase KRas, which are found in over 90% of PDAC tumours, a contributory factor for PDAC tumour progression is formation of a rigid extracellular matrix (ECM) and associated desmoplasia. This response leads to aberrant integr ...[more]

PMID: 35405272

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Project description:Cholangiocarcinoma (CCA) is a hepatobiliary malignancy with dismal prognosis. Currently available models fail to recapitulate the full complexity of CCA, particularly the desmoplastic environment and the interplay between cancer cells and the extracellular matrix (ECM). We aimed to study the role of epithelial tumor cells in ECM deposition and desmoplasia by designing a model encompassing primary epithelial CCA organoids (CCAOs) and native liver and tumor scaffolds obtained by decellularization Background & Aims: Cholangiocarcinoma (CCA) is a hepatobiliary malignancy with dismal prognosis. Currently available models fail to recapitulate the full complexity of CCA, particularly the desmoplastic environment and the interplay between cancer cells and the extracellular matrix (ECM). We aimed to study the role of epithelial tumor cells in ECM deposition and desmoplasia by designing a model encompassing primary epithelial CCA organoids (CCAOs) and native liver and tumor scaffolds obtained by decellularization. Results: Decellularization resulted in effective removal of cells while preserving ECM structure and retaining important characteristics of the tissue origin. When culturing CCAOs in CCA-M, compared to TFL-M and BME, the genome-wide gene expression profile much more resembled the transcriptome of primary CCA tumor tissue in vivo, with an accompanying increase in chemoresistance. CCAOs in decellularized matrix, both CCA-M and TFL-M, exhibited the formation of complex morphological structures, and revealed environment-dependent proliferation and migration dynamics, driven by the occurrence of epithelial-mesenchymal transition (EMT). CCA-M induced specific extracellular matrix protein production in CCAOs, such as fibronectin 1 (FN1), which is related to desmoplasia and patient survival. In TFL-M, lacking the desmoplastic environment, CCAOs were able to initiate a desmoplastic reaction directly through increased production of multiple collagen types. Conclusions: This improved model of cholangiocarcinoma, combining organoids and native extracellular matrix, recapitulates key components of CCA tumor biology, including transcriptome profiles, migration patterns, EMT, and ECM protein production. The increased production of extracellular matrix proteins suggests that epithelial tumor cells can contribute to their own desmoplastic environment.