Jennifer Lothion-Roy
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jennifer Lothion-Roy has a total of 21 co-authors. Here are the top co-authors by number of shared publications:
- Anna E. Harris
Biodiscovery Institute, University of Nottingham, Nottingham, UK
1 shared publication - Atara Ntekim
College of Medicine, University of Ibadan, Ibadan, Nigeria
1 shared publication - Brian D. Robinson
Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, USA
1 shared publication - Catrin Sian Rutland
School of Veterinary Medicine and Sciences, Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham LE12 5RD, UK
1 shared publication - Corinne L. Woodcock
School of Veterinary Medicine and Science, Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham LE12 5RD, UK
1 shared publication - Daisy B. Haigh
Biodiscovery Institute, University of Nottingham, University Park, Nottingham NG7 2RD, UK
1 shared publication
Latest Publications
- Open Access
The METTL3 RNA Methyltransferase Regulates Transcriptional Networks in Prostate Cancer
Prostate cancer (PCa) is a leading cause of cancer-related deaths and is driven by aberrant androgen receptor (AR) signalling. For this reason, androgen deprivation therapies (ADTs) that suppress androgen-induced PCa progression either by preventing androgen biosynthesis or via AR signalling inhibition (ARSi) are common treatments. The N6-methyladenosine (m6A) RNA modification is involved in regulating mRNA expression, translation, and alternative splicing, and through these mechanisms has been implicated in cancer development and progression. RNA-m6A is dynamically regulated by the METTL3 RNA methyltransferase complex and the FTO and ALKBH5 demethylases. While there is evidence supporting a role for aberrant METTL3 in many cancer types, including localised PCa, the wider contribution of METTL3, and by inference m6A, in androgen signalling in PCa remains poorly understood. Therefore, the aim of this study was to investigate the expression of METTL3 in PCa patients and study the clinical and functional relevance of METTL3 in PCa. It was found that METTL3 is aberrantly expressed in PCa patient samples and that siRNA-mediated METTL3 knockdown or METTL3-pharmacological inhibition significantly alters the basal and androgen-regulated transcriptome in PCa, which supports targeting m6A as a novel approach to modulate androgen signalling in PCa.
Open AccessThe METTL3 RNA Methyltransferase Regulates Transcriptional Networks in Prostate Cancer
Prostate cancer (PCa) is a leading cause of cancer-related deaths and is driven by aberrant androgen receptor (AR) signalling. For this reason, androgen deprivation therapies (ADTs) that suppress androgen-induced PCa progression either by preventing androgen biosynthesis or via AR signalling inhibition (ARSi) are common treatments. The N6-methyladenosine (m6A) RNA modification is involved in regulating mRNA expression, translation, and alternative splicing, and through these mechanisms has been implicated in cancer development and progression. RNA-m6A is dynamically regulated by the METTL3 RNA methyltransferase complex and the FTO and ALKBH5 demethylases. While there is evidence supporting a role for aberrant METTL3 in many cancer types, including localised PCa, the wider contribution of METTL3, and by inference m6A, in androgen signalling in PCa remains poorly understood. Therefore, the aim of this study was to investigate the expression of METTL3 in PCa patients and study the clinical and functional relevance of METTL3 in PCa. It was found that METTL3 is aberrantly expressed in PCa patient samples and that siRNA-mediated METTL3 knockdown or METTL3-pharmacological inhibition significantly alters the basal and androgen-regulated transcriptome in PCa, which supports targeting m6A as a novel approach to modulate androgen signalling in PCa.