Professor Jim Boyne
Head of Subject | Leeds Beckett
Leeds, UNITED KINGDOM
Jim Boyne's laboratory investigates the role of RNA in human disease.
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Biography
Professor Boyne began his research career at The University of Sheffield working on cell cycle control before completing postdoctoral research posts at Cancer Research UK and the University of Leeds, investigating cancer signalling and oncogenic viruses, respectively.
He took up his first academic position at the University of Bradford in 2009, where he established a successful cancer research group as PI and eventually took on the role of Director of Postgraduate Research. In 2018, he moved to the University of Huddersfield as Reader in Cancer Research, where he secured external funding to establish a melanoma research group. In 2021, he joined Leeds Beckett University as Head of Biomedical Science, and was promoted to Professor of Cancer Research in 2022.
Work in Professor Boyne's laboratory investigates the role of RNA in human disease, focusing on the utility of cell-free RNAs as liquid biomarkers for cancer progression and healthy ageing. His main research audience are scientists and clinicians interested in understanding how genetics contribute to human disease.
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Molecular & Cellular Biology
Cancer Research
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- English
Articles (3)
SFPQ promotes an oncogenic transcriptomic state in melanoma
Oncogene2021 The multifunctional protein, splicing factor, proline- and glutamine-rich (SFPQ) has been implicated in numerous cancers often due to interaction with coding and non-coding RNAs, however, its role in melanoma remains unclear. We report that knockdown of SFPQ expression in melanoma cells decelerates several cancer-associated cell phenotypes, including cell growth, migration, epithelial to mesenchymal transition, apoptosis, and glycolysis. RIP-seq analysis revealed that the SFPQ-RNA interactome is reprogrammed in melanoma cells and specifically enriched with key melanoma-associated coding and long non-coding transcripts, including SOX10, AMIGO2 and LINC00511 and in most cases SFPQ is required for the efficient expression of these genes.
The role of CAF derived exosomal microRNAs in the tumour microenvironment of melanoma
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer2021 Exosomes play a crucial role in the crosstalk between cancer associated fibroblasts (CAFs) and cancer cells, contributing to carcinogenesis and the tumour microenvironment. Recent studies have revealed that CAFs, normal fibroblasts and cancer cells all secrete exosomes that contain miRNA, establishing a cell-cell communication network within the tumour microenvironment. For example, miRNA dysregulation in melanoma has been shown to promote CAF activation via induction of epithelial-mesenchymal transition (EMT), which in turn alters the secretory phenotype of CAFs in the stroma. This review assesses the roles of melanoma exosomal miRNAs in CAF formation and how CAF exosome-mediated feedback signalling to melanoma lead to tumour progression and metastasis.
MCV-miR-M1 Targets the Host-Cell Immune Response Resulting in the Attenuation of Neutrophil Chemotaxis
Journal of Infectious Diseases2018 Virus-encoded microRNAs are emerging as key regulators of persistent infection and host-cell immune evasion. Merkel cell polyomavirus, the predominant etiological agent of Merkel cell carcinoma, encodes a single microRNA, MCV-miR-M1, which targets the oncogenic Merkel cell polyomavirus large T antigen. MCV-miR-M1 has previously been shown to play an important role in the establishment of long-term infection, however, the underlying mechanism is not fully understood. A key unanswered question is whether, in addition to autoregulating large T antigen, MCV-miR-M1 also targets cellular transcripts to orchestrate an environment conducive to persistent infection. To address this, we adopted an RNA sequencing–based approach to identify cellular targets of MCV-miR-M1. Intriguingly, bioinformatics analysis of transcripts that are differentially expressed in cells expressing MCV-miR-M1 revealed several genes implicated in immune evasion.
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