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Molecular & Cellular Oncology Volume 5, 2018 - Issue 5
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Commentary

Ubiquitination and adaptive responses to BRAF inhibitors in Melanoma

Azad SaeiGenome Institute of Singapore, A*STAR, Singapore;Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, SingaporeCorrespondence[email protected]
ORCID Iconhttp://orcid.org/0000-0002-1000-2953View further author information
ORCID Icon &
Pieter Johan Adam EichhornCancer Science Institute of Singapore, National University of Singapore, Singapore;Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore;School of Pharmacy and Biomedical Sciences, Curtin University, Perth, AustraliaORCID Iconhttp://orcid.org/0000-0001-5840-943XView further author information
ORCID Icon
Article: e1497862 | Received 29 Jun 2018, Accepted 04 Jul 2018, Published online: 05 Sep 2018

Figures & data

Figure 1. Vemurafenib resistance in melanoma cells lacking USP28. Under normal conditions ubiquitin specific peptidase 28 (USP28) functions to stabilise F-box WD repeat-containing protein 7 (FBW7) resulting in SKP1/CUL1/F-box (SCF) mediated downregulation of targeted substrates including v-raf murine sarcoma viral oncogene homolog B (BRAF, left panel). Under USP28 depleted conditions BRAF stabilisation enhances mitogen-activated protein kinas (MAPK) pathway activation and resistance to BRAF inhibitors (right panel).

Figure 1. Vemurafenib resistance in melanoma cells lacking USP28. Under normal conditions ubiquitin specific peptidase 28 (USP28) functions to stabilise F-box WD repeat-containing protein 7 (FBW7) resulting in SKP1/CUL1/F-box (SCF) mediated downregulation of targeted substrates including v-raf murine sarcoma viral oncogene homolog B (BRAF, left panel). Under USP28 depleted conditions BRAF stabilisation enhances mitogen-activated protein kinas (MAPK) pathway activation and resistance to BRAF inhibitors (right panel).

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