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A highly potent bi-thiazole inhibitor of LOX rewires collagen architecture and enhances chemoresponse in triple-negative breast cancer

ABSTRACT: Matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI) data investigating changes in extracellular matrix/collagen architecture of mouse tumor tissue in response to LOX inhibition. Sample Key: Vehicle, Doxo (Chemotherapy drug), 6403 (LOX inhibitor), Combo (Doxo + LOX inhibitor)

INSTRUMENT(S): Bruker Daltonics instrument model

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Breast

DISEASE(S): Breast Cancer

SUBMITTER: Peggi Angel

LAB HEAD: Harrison Taylor

PROVIDER: PXD052657 | Pride | 2024-07-25

REPOSITORIES: Pride

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			Action	DRS
	20230201_Mus_Ozgur.fasta	Fasta
	2024_Metinetal_LOXinhibitorExp.mzXML	Mzxml
	checksum.txt	Txt
	identifiedPeptides.Data	Other

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A highly potent bi-thiazole inhibitor of LOX rewires collagen architecture and enhances chemoresponse in triple-negative breast cancer

Project description:Raw proteomic files Metin C, Saatci O, Rezaeian A-H, Rao CN, Beneker C, Taylor H, Pederson B, Chatzistamou I, Buckley B, Lessner S, Angel P, McInnes C, Sahin O. A highly potent bi-thiazole inhibitor of LOX rewires collagen architecture and enhances chemoresponse in triple-negative breast cancer. Cell Chem Biol

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Defining the Tumor Microenvironment by Integration of Im-munohistochemistry and Extracellular Matrix Targeted Imaging Mass Spectrometry

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Electron Capture vs. Transfer Dissociation for Site Determination of Tryptic Peptide Tyrosine Sulfation: Direct Detection of Fibrinogen Sulfation Sites and Identification of Novel Isobaric Interferences

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proteome analysis of Nilaparvata lugens cuticle

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Effect of LOX-PP on the gene expression profile of the A673 cell line (Ewing sarcoma)

Project description:In this study we show that lysyl oxidase (LOX), an enzyme involved in maintaining structural integrity of the extracellular matrix, is expressed at low levels in Ewing sarcoma cells and primary tumors and is downregulated by the EWS/FLI1 oncoprotein characteristic of these tumors. Using a doxycycline inducible system to restore LOX expression in an Ewing sarcoma derived cell line, we show that LOX displays tumor suppressor activities. Interestingly, we show that the tumor suppressor activity resides in the propeptide domain of LOX (LOX-PP), an N-terminal domain produced by proteolytic cleavage during the physiological processing of LOX. Finally, we show that LOX-PP inhibits ERK/MAPK signalling pathway, and that many pathways involved in cell cycle progression were significant deregulated by LOX-PP, providing a mechanistic explanation to the cell proliferation inhibition observed upon LOX-PP expression. In summary, our observations indicate that deregulation of the LOX gene participates in Ewing sarcoma development and identify LOX-PP as a new therapeutic target for one of the most aggressive paediatric malignancies. These findings suggest that therapeutic strategies based in the administration of LOX propeptide or functional analogues could be useful in the treatment of this devastating paediatric cancer.

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