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- W2022164698 abstract "activated in cancer and whether its modulation may have an effect on cancer. Materials and Methods: LysRS status was analyzed by using protein fractionation assays as described by Yannay-Cohen et al. We used Hela cells and H460 cells overexpressing EGFR generously provided by G. Batist (Mcgill U. Montreal) to study possible relationship to the EGFR pathway. Hint constructs were cotransfected with wildtype or mutant LYSRS encoding constructs to A549 lung cancer cells. Results: We checked EGFR effects on this pathway − EGF activation of HELA cells resulted in movement of LysRS to smaller protein fractions implying release of LysRS from the multisynthetase comple. Inhibition with Gefitinib of EGFR in a NSCLCA line resulted in the opposite effect. MAPK inhibition resulted in the disappearance of LysRS from smaller protein fractions in a cell line with overactivated MAPK pathway, implying that the presence of LysRS in smaller complexes can be manipulated by MAPK inhibition. Transfection of S207DLys RS pseudophosphorylated mimic with HINT1 prevented HINT1 activity as a tumour suppressor in a colony assay of A549 cells. Conclusion: Our results suggest that the lysRS-AP4A pathway is activated in cancer. Activation of such a pathway in cancer might have distinct effects as shown in the case of HINT1tumour suppression. This is the first demonstration of the activity of this pathway in cancer. Other signal transduction pathway operating according to the principles of the depot theory may be aberrantly overactivated in cancer. Further research is needed to delineate the precise biological significance of this pathway in different cancers." @default.
- W2022164698 created "2016-06-24" @default.
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- W2022164698 date "2011-09-01" @default.
- W2022164698 modified "2023-09-26" @default.
- W2022164698 title "1044 POSTER Acquisition of P-glycoprotein Overexpression in Sensitive Tumour Cells" @default.
- W2022164698 doi "https://doi.org/10.1016/s0959-8049(11)70687-6" @default.
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