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A System-wide Approach to Monitor Responses to Synergistic BRAF and EGFR Inhibition in Colorectal Cancer Cells
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- Ressa, Anna (författare)
- Univ Utrecht, Utrecht Inst Pharmaceut Sci, Biomol Mass Spectrometry & Prote Grp, Padualaan 8, NL-3584 CH Utrecht, Netherlands.
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- Bosdriesz, Evert (författare)
- Netherlands Canc Inst, Oncode Inst, Canc Genom Ctr Netherlands, Div Mol Carcinogenesis, Plesmanlaan 121, NL-1066 CX Amsterdam, Netherlands.
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- de Ligt, Joep (författare)
- Univ Utrecht, Univ Med Ctr Utrecht, Div Biomed Genet, Ctr Mol Med & Canc Genom Netherlands, Univ Weg 100, NL-3584 CG Utrecht, Netherlands.
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- Univ Utrecht, Utrecht Inst Pharmaceut Sci, Biomol Mass Spectrometry & Prote Grp, Padualaan 8, NL-3584 CH Utrecht, Netherlands Netherlands Canc Inst, Oncode Inst, Canc Genom Ctr Netherlands, Div Mol Carcinogenesis, Plesmanlaan 121, NL-1066 CX Amsterdam, Netherlands. (creator_code:org_t)
- AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2018
- 2018
- Engelska.
- Ingår i: Molecular & Cellular Proteomics. - : AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC. - 1535-9476 .- 1535-9484. ; 17:10, s. 1892-1908
- Tidskriftsartikel (refereegranskat)
Abstract
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- Intrinsic and/or acquired resistance represents one of the great challenges in targeted cancer therapy. A deeper understanding of the molecular biology of cancer has resulted in more efficient strategies, where one or multiple drugs are adopted in novel therapies to tackle resistance. This beneficial effect of using combination treatments has also been observed in colorectal cancer patients harboring the BRAF(V600E) mutation, whereby dual inhibition of BRAF(V600E) and EGFR increases antitumor activity. Notwithstanding this success, it is not clear whether this combination treatment is the only or most effective treatment to block intrinsic resistance to BRAF inhibitors. Here, we investigate molecular responses upon single and multi-target treatments, over time, using BRAF(V600E) mutant colorectal cancer cells as a model system. Through integration of transcriptomic, proteomic and phosphoproteomics data we obtain a comprehensive overview, revealing both known and novel responses. We primarily observe widespread up-regulation of receptor tyrosine kinases and metabolic pathways upon BRAF inhibition. These findings point to mechanisms by which the drug-treated cells switch energy sources and enter a quiescent-like state as a defensive response, while additionally compensating for the MAPK pathway inhibition.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine (hsv//eng)
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- Ressa, Anna
- Bosdriesz, Evert
- de Ligt, Joep
- Mainardi, Sara
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- Groten, Stijn
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- Bernards, Rene
- Cuppen, Edwin
- Wessels, Lodewyk
- Heck, Albert J. ...
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