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MEK and PI3K resistant proteome of pancreatic cancer cells

ABSTRACT: MEK and PI3K inhibition on pancreatic cancer cells has demonstrated the existence of intrinsic resistance. Therefore, a comprehensive proteome profiling is needed to understand the associated molecular phenotype. PANC-1 and MIA PaCa-2 cancer cells were studied by label-free data-independent acquisition (SWATH) mass spectrometry with extensive peptide fractionation to quantitate and reveal differential expression of several proteins between resistant and sensitive cells. Proteomic differences cover a broad scope of molecular processes and putative candidate proteins for drug response.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Pancreas

DISEASE(S): Pancreas Adenocarcinoma

SUBMITTER: Juan Francisco Martinez-Aguilar

LAB HEAD: Juan Francisco

PROVIDER: PXD016493 | Pride | 2025-03-10

REPOSITORIES: Pride

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Source:

			Action	DRS
	190601_Micro_MiaPaCa_SWATH_1.1.wiff	Wiff
	190601_Micro_MiaPaCa_SWATH_1.1.wiff.scan	Wiff
	190601_Micro_MiaPaCa_SWATH_2.wiff	Wiff
	190601_Micro_MiaPaCa_SWATH_2.wiff.scan	Wiff
	190601_Micro_MiaPaCa_SWATH_3.wiff	Wiff

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Project description:Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.

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MEK and PI3K resistant proteome of pancreatic cancer cells

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