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MAP2K1 is a potential therapeutic target in erlotinib resistant head and neck squamous cell carcinoma. 2019
Ankit P Jain, and
Krishna Patel, and
Sneha Pinto, and
Aneesha Radhakrishnan, and
Vishalakshi Nanjappa, and
Manish Kumar, and
Remya Raja, and
Arun H Patil, and
Anjali Kumari, and
Malini Manoharan, and
Coral Karunakaran, and
Saktivel Murugan, and
T S Keshava Prasad, and
Xiaofei Chang, and
Premendu Prakash Mathur, and
Prashant Kumar, and
Ravi Gupta, and
Rohit Gupta, and
Arati Khanna-Gupta, and
David Sidransky, and
Aditi Chatterjee, and
Harsha Gowda
Institute of Bioinformatics, International Technology Park, Bangalore, 560066, India.
Epidermal growth factor receptor (EGFR) targeted therapies have shown limited efficacy in head and neck squamous cell carcinoma (HNSCC) patients despite its overexpression. Identifying molecular mechanisms associated with acquired resistance to EGFR-TKIs such as erlotinib remains an unmet need and a therapeutic challenge. In this study, we employed an integrated multi-omics approach to delineate mechanisms associated with acquired resistance to erlotinib by carrying out whole exome sequencing, quantitative proteomic and phosphoproteomic profiling. We observed amplification of several genes including AXL kinase and transcription factor YAP1 resulting in protein overexpression. We also observed expression of constitutively active mutant MAP2K1 (p.K57E) in erlotinib resistant SCC-R cells. An integrated analysis of genomic, proteomic and phosphoproteomic data revealed alterations in MAPK pathway and its downstream targets in SCC-R cells. We demonstrate that erlotinib-resistant cells are sensitive to MAPK pathway inhibition. This study revealed multiple genetic, proteomic and phosphoproteomic alterations associated with erlotinib resistant SCC-R cells. Our data indicates that therapeutic targeting of MAPK pathway is an effective strategy for treating erlotinib-resistant HNSCC tumors.
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