Contact information
Old Road Campus Research Building
Colin Goding
Professor of Oncology
I completed a PhD in virology at the National Institute for Medical Research, London, UK. I then did postdoctoral work in Pierre Chambon’s lab in Strasbourg, France, where I developed an interest in transcription regulation before taking up a position at the Marie Curie Research Institute, Oxted, UK, to continue working on gene regulation, both in S. cerevisiae, as well as in melanocytes and melanoma. In 2008, I moved to the Ludwig Institute, where I continue to examine the role of signalling and transcription in melanoma biology, with the aim of developing novel and anti-cancer therapies that take tumour phenotypic heterogeneity into account.
Using melanoma as a model, we established the key role of the Microphthalmia-associated transcription factor (MITF) in microenvironment-driven phenotype-switching in melanoma biology: MITF-low cells are drug-resistant, slow-cycling, tumour-initiating and invasive, while MITF expression suppresses invasiveness and promotes either proliferation or differentiation. Understanding how MITF is regulated, both transcriptionally and post-translationally, and how it integrates microenvironmental signals to determine melanoma phenotype is a key aim. More broadly, we are interested in how and why invasiveness is imposed and stem cells generated in melanoma, and how similar phenotypic states are produced in non-melanoma cancers.
To explain cancer progression we recently introduced the concept of starvation and pseudo-starvation to explain why cancer cells become invasive.
Our research is therefore aimed at understanding:
- The drivers of phenotype-switching and senescence
- The role of starvation and pseudo-starvation in cancer progression
- The relationship between invasiveness and tumour initiation
- The molecular mechanisms underpinning dormancy
- The role of MITF-related factors in non-melanoma cancers
Key publications
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Starvation and Pseudo-Starvation as Drivers of Cancer Metastasis through Translation Reprogramming.
Journal article
García-Jiménez C. and Goding CR., (2019), Cell metabolism, 29, 254 - 267
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BRN2 suppresses apoptosis, reprograms DNA damage repair, and is associated with a high somatic mutation burden in melanoma.
Journal article
Herbert K. et al, (2019), Genes & development, 33, 310 - 332
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Targeting MC1R depalmitoylation to prevent melanomagenesis in redheads.
Journal article
Chen S. et al, (2019), Nature communications, 10
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A TFEB nuclear export signal integrates amino acid supply and glucose availability
Journal article
Li L. et al, (2018), Nature Communications, 9
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Translation reprogramming is an evolutionarily conserved driver of phenotypic plasticity and therapeutic resistance in melanoma
Journal article
Falletta P. et al, (2017), Genes & Development, 31, 18 - 33
Recent publications
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TPC1 regulates melanoma tumourigenesis via mTORC1 and TFEB.
Journal article
Jin X. et al, (2024), Heliyon, 10
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The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State
Journal article
Johns E. et al, (2024), Pigment Cell & Melanoma Research