Mining gastric cancer cellular quantitative phosphotyrosine proteomics data to analyse the signiling cascade regulated my CAMKK2 in gastric cancer

Gastric cancer is a global health concern. Tyrosine kinases (TKs) are important mediators of signaling cascades, which regulate diverse biological processes like growth, differentiation, metabolism, and apoptosis in response to external and internal stimuli. Molecular alterations in various signaling pathways have been implicated in the development and late-stage progression/metastasis of gastric cancer. Dysregulation of TK’s are reported to be involved in different malignancies.1 Tyrosine kinases represent a major portion of all oncoproteins that play a transforming role in a plethora of cancers.. This study aimed at analysing the phosphotyrosine proteome change upon inhibition of CAMKK2 in gastric cancer cells using LC-MS/MS based quantitative inhibition proteomic approach. A label free based quantitative approach was used to identify the significantly altered phosphorylations upon inhibition of CAMKK2. Gene Ontology (GO) analysis and pathway analysis was done for the significantly altered proteins and was later validated by immunoblotting.