Dataset Information

Effects of AKT inhibition in the pancreatic cancer cell proteome

ABSTRACT: The AKT pathway is a major regulator of human pancreatic adenocarcinoma progression and a key pharmacological target. The mechanisms of adaptation to long-term silencing of AKT isoforms of human and mouse pancreatic adenocarcinoma cancer cells were studied.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Pancreas

DISEASE(S): Pancreas Adenocarcinoma

SUBMITTER: Enrique SantamarÃa

LAB HEAD: Enrique Santamaria

PROVIDER: PXD020673 | Pride | 2021-09-09

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	100mM-105-iTRAQCito-20102016-10.wiff	Wiff
	100mM-105-iTRAQCito-20102016-10.wiff.scan	Wiff
	10mM-105-iTRAQCito-20102016-1.wiff	Wiff
	10mM-105-iTRAQCito-20102016-1.wiff.scan	Wiff
	10mM-105-iTRAQCito-20102016-11.group	Other

Items per page:

1 - 5 of 26

Publications

Profound Reprogramming towards Stemness in Pancreatic Cancer Cells as Adaptation to AKT Inhibition.

Arasanz Hugo H Hernández Carlos C Bocanegra Ana A Chocarro Luisa L Zuazo Miren M Gato Maria M Ausin Karina K Santamaría Enrique E Fernández-Irigoyen Joaquín J Fernandez Gonzalo G Santamaria Eva E Rodríguez Carlos C Blanco-Luquin Idoia I Vera Ruth R Escors David D Kochan Grazyna G

Cancers 20200805 8

Cancer cells acquire resistance to cytotoxic therapies targeting major survival pathways by adapting their metabolism. The AKT pathway is a major regulator of human pancreatic adenocarcinoma progression and a key pharmacological target. The mechanisms of adaptation to long-term silencing of AKT isoforms of human and mouse pancreatic adenocarcinoma cancer cells were studied. Following silencing, cancer cells remained quiescent for long periods of time, after which they recovered proliferative cap ...[more]

PMID: 32764385

Similar Datasets

Project description:Background: Results obtained from our previous study using a label-free quantitation (LF) proteomic approach in which dynamic range compression was used to profile lower abundance proteins, demonstrated few proteins that were differentially abundant within the synovial fluid (SF) when comparing Autologous Chondrocyte Implantation (ACI) responders and non-responders at baseline (1). This study builds upon our previous findings by assessing higher abundance proteins within these SFs; providing a more global proteome analysis from which we can understand more fully the biology underlying ACI success or failure. Methods: Isobaric tagging for relative and absolute quantitation (iTRAQ) proteomics was used to assess SFs from ACI responders (mean Lysholm improvement of 33; n=14) and non-responders (mean Lysholm decrease of 14; n=13) at the two stages of surgery (cartilage harvest and chondrocyte implantation). Differentially abundant proteins were investigated using pathway analyses and the iTRAQ proteomic dataset was combined with our published proteomic dataset of dynamically compressed SFs, from which an interactome network model of systemic protein interactions was generated. Results: iTRAQ proteomics has confirmed our previous finding that there is a marked proteome shift in response to cartilage harvest (70 and 54 proteins demonstrating ≥2.0 fold change between Stages I and II in responders and non-responders, respectively) and has highlighted 28 proteins that were differentially abundant between responders and non-responders to ACI, that were not found in the LF study; 16 of which were altered at baseline. Two protein abundance changes (Complement C1S subcomponent and Matrix metalloproteinase 3 (MMP3), have been biochemically validated. Combination of the iTRAQ and LF proteomic datasets has generated in-depth SF proteome information that has been used to generate interactome networks representing ACI success or failure, from which functional pathways that are dysregulated in ACI non-responders have been identified. Conclusions: Several candidate biomarkers for baseline prediction of ACI outcome have been identified. A holistic overview of the SF proteome in responders and non-responders to ACI has been profiled providing a better understanding of the biological pathways underlying clinical outcome, particularly the differential response to cartilage harvest in non-responders.