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Identification of Serum Metabolite Biomarkers and Metabolic Reprogramming Mechanisms to Predict Recurrence in Cholangiocarcinoma

ABSTRACT: Cholangiocarcinoma (CCA) has high recurrence rates that severely limit long-term survival. Effective tools for accurate recurrence monitoring and diagnosis remain lacking. Metabolic reprogramming, a key driver of CCA growth and recurrence, is underutilized in cancer screening and management. This study aimed to identify metabolite-based biomarkers to evaluate recurrence severity, enhance disease management, and elucidate the molecular mechanisms underlying CCA recurrence.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Watcharin Loilome

PROVIDER: PXD060214 | JPOST Repository | Wed Mar 19 00:00:00 GMT 2025

REPOSITORIES: jPOST

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			Action	DRS
	20240915_R1_Blank01.mgf	Mgf
	20240915_R1_Blank01.mzXML	Mzxml
	20240920_R3_Met-Pos_S74.mzXML	Mzxml
	20240920_R3_Met-Pos_S75.mzXML	Mzxml
	20240920_R3_Met-Pos_S76.mzXML	Mzxml

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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.

Dataset Information

Identification of Serum Metabolite Biomarkers and Metabolic Reprogramming Mechanisms to Predict Recurrence in Cholangiocarcinoma

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