ArticleCancer management and research2020
Quantitative Tyrosine Phosphoproteomic Analysis of Resistance to Radiotherapy in Nasopharyngeal Carcinoma Cells.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- A transcriptomic analysis based on aberrant methylation levels revealed potential novel therapeutic targets for nasopharyngeal carcinoma.Annals of translational medicine · 2022Article
- Phosphoproteomics: a valuable tool for uncovering molecular signaling in cancer cells.Expert review of proteomics · 2021Review
- The Role of Myeloid-Derived Suppressor Cells in the Treatment of Pancreatic Cancer.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRadioresistance poses a major challenge in nasopharyngeal carcinoma (NPC) treatment. Protein tyrosine phosphorylation has emerged as a key device in the control of resistance to therapy in cancer cells.
methodsUsing tandem mass tag (TMT) labeling and phospho-antibody affinity enrichment followed by high-resolution LC-MS/MS analysis, quantitative tyrosine phosphorylome analysis was performed in CNE2 (parental) and its radioresistant subline CNE2-IR.
resultsAltogether, 233 tyrosine phosphorylation sites in 179 protein groups were identified, among which 179 sites in 140 proteins were quantified. Among the quantified proteins, 38 tyrosine phosphorylation proteins are up-regulated and 18 tyrosine phosphorylation proteins are down-regulated in CNE2-IR vs CNE2. Increased tyrosine phosphorylation in multiple receptor/protein tyrosine kinases (EPHA2, EGFR, IGF1R, ABL1 and LYN) was identified in CNE2-IR vs CNE2 cells. Intensive bioinformatic analyses revealed robust activation of multiple biological processes/pathways including E-cadherin stabilization, cell-cell adhesion, and cell junction organization in radioresistant CNE2-IR cells. Specifically, we observed that the CNE2 cells incubated with EphrinA1-Fc exhibited higher EPHA2 Y772 phosphorylation and lower E-cadherin expression, as compared with PBS control. Furthermore, an ATP-competitive EPHA2 RTK inhibitor (ALW-II-41-27, ALW) reduced EPHA2 Y772 phosphorylation and increased the expression of E-cadherin in CNE2-IR cells. Colony formation analysis showed that EFNA1 (EFNA1 is the ligand of EPHA2) treatment in CNE2 significantly promoted colony formation after 6Gy irradiation; while incubation with EPHA2 inhibitor ALW-II-41-27 in CNE2-IR cells impaired colony formation after irradiation, as compared with solvent control (DMSO).
conclusionIn conclusion, phosphoproteomic approach allowed us to link tyrosine kinases signaling with radioresistance in NPC. Further studies are necessary to delineate the molecular function of EPHA2/E-cadherin signaling in radioresistant NPC and to explore rational combination therapy and its underlying mechanism.
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