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  1. Article: Effects of a Football Simulated Exercise on Injury Risk Factors for Anterior Cruciate Ligament (ACL) Injury in Amateur Female Players.

    Ferguson, Harriet / Piquet, Jessica / Jemni, Monèm / Delextrat, Anne

    Biology

    2023  Volume 12, Issue 1

    Abstract: Females are more at risk of Anterior Cruciate Ligament (ACL) injuries than males; however, there is limited literature on neuromuscular risk factors such as angle-specific hamstring/quadriceps functional strength ratios ( ... ...

    Abstract Females are more at risk of Anterior Cruciate Ligament (ACL) injuries than males; however, there is limited literature on neuromuscular risk factors such as angle-specific hamstring/quadriceps functional strength ratios (H
    Language English
    Publishing date 2023-01-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12010124
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Effects of a Football Simulated Exercise on Injury Risk Factors for Anterior Cruciate Ligament (ACL) Injury in Amateur Female Players

    Ferguson, Harriet / Piquet, Jessica / Jemni, Monem / Delextrat, Anne

    Biology (Basel). 2023 Jan. 12, v. 12, no. 1

    2023  

    Abstract: Females are more at risk of Anterior Cruciate Ligament (ACL) injuries than males; however, there is limited literature on neuromuscular risk factors such as angle-specific hamstring/quadriceps functional strength ratios (Hₑcc/Qcₒₙ) and rate of torque ... ...

    Abstract Females are more at risk of Anterior Cruciate Ligament (ACL) injuries than males; however, there is limited literature on neuromuscular risk factors such as angle-specific hamstring/quadriceps functional strength ratios (Hₑcc/Qcₒₙ) and rate of torque development (RTD) in female footballers. The aim of this study was to investigate the effects of fatigue on these neuromuscular risk factors. Thirty-three amateur players (20.3 ± 2.0 years old, 1.67 ± 9.31 m, 63.4 ±8.1 kg, 23.6 ± 5.7% body fat) performed strength assessments of the quadriceps (concentrically, Qcₒₙ) and hamstrings (eccentrically, Hₑcc) on both legs on an isokinetic dynamometer, before and immediately after a football-specific exercise. Results showed significantly lower peak Hₑcc (−15.1 to −15.5%), peak Hₑcc/Qcₒₙ (−8.8 to −12.9%) and RTD (−14.0 to −17.0%) for hamstring eccentric contractions after fatigue in the dominant and non-dominant legs. Furthermore, significant decreases in Hₑcc/Qcₒₙ were observed at 10° only in the dominant leg (−15.5%), and at 10°, 20° and 30° in the non-dominant leg (−15.1 to −21.8%). These results suggest a reduced capacity of the hamstrings to stabilise the knee joint with fatigue. Unlike results previously shown on men, the non-dominant leg seemed more affected, highlighting the need to consider specific prevention measures in females.
    Keywords anterior cruciate ligament ; body fat ; exercise ; females ; risk ; torque
    Language English
    Dates of publication 2023-0112
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article ; Online
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12010124
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.

    Ferguson, Harriet R / Smith, Michael P / Francavilla, Chiara

    Cells

    2021  Volume 10, Issue 5

    Abstract: Increasing evidence indicates that success of targeted therapies in the treatment of cancer is context-dependent and is influenced by a complex crosstalk between signaling pathways and between cell types in the tumor. The Fibroblast Growth Factor (FGF)/ ... ...

    Abstract Increasing evidence indicates that success of targeted therapies in the treatment of cancer is context-dependent and is influenced by a complex crosstalk between signaling pathways and between cell types in the tumor. The Fibroblast Growth Factor (FGF)/FGF receptor (FGFR) signaling axis highlights the importance of such context-dependent signaling in cancer. Aberrant FGFR signaling has been characterized in almost all cancer types, most commonly non-small cell lung cancer (NSCLC), breast cancer, glioblastoma, prostate cancer and gastrointestinal cancer. This occurs primarily through amplification and over-expression of
    MeSH term(s) Carcinogenesis ; Humans ; Neoplasms/metabolism ; Receptor, Fibroblast Growth Factor, Type 1/metabolism ; Receptor, Fibroblast Growth Factor, Type 2/metabolism
    Chemical Substances FGFR1 protein, human (EC 2.7.10.1) ; FGFR2 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1)
    Language English
    Publishing date 2021-05-14
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10051201
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Oxidative stress from DGAT1 oncoprotein inhibition in melanoma suppresses tumor growth when ROS defenses are also breached.

    Wilcock, Daniel J / Badrock, Andrew P / Wong, Chun W / Owen, Rhys / Guerin, Melissa / Southam, Andrew D / Johnston, Hannah / Telfer, Brian A / Fullwood, Paul / Watson, Joanne / Ferguson, Harriet / Ferguson, Jennifer / Lloyd, Gavin R / Jankevics, Andris / Dunn, Warwick B / Wellbrock, Claudia / Lorigan, Paul / Ceol, Craig / Francavilla, Chiara /
    Smith, Michael P / Hurlstone, Adam F L

    Cell reports

    2024  Volume 39, Issue 12, Page(s) 110995

    Abstract: Dysregulated cellular metabolism is a cancer hallmark for which few druggable oncoprotein targets have been identified. Increased fatty acid (FA) acquisition allows cancer cells to meet their heightened membrane biogenesis, bioenergy, and signaling needs. ...

    Abstract Dysregulated cellular metabolism is a cancer hallmark for which few druggable oncoprotein targets have been identified. Increased fatty acid (FA) acquisition allows cancer cells to meet their heightened membrane biogenesis, bioenergy, and signaling needs. Excess FAs are toxic to non-transformed cells but surprisingly not to cancer cells. Molecules underlying this cancer adaptation may provide alternative drug targets. Here, we demonstrate that diacylglycerol O-acyltransferase 1 (DGAT1), an enzyme integral to triacylglyceride synthesis and lipid droplet formation, is frequently up-regulated in melanoma, allowing melanoma cells to tolerate excess FA. DGAT1 over-expression alone transforms p53-mutant zebrafish melanocytes and co-operates with oncogenic BRAF or NRAS for more rapid melanoma formation. Antagonism of DGAT1 induces oxidative stress in melanoma cells, which adapt by up-regulating cellular reactive oxygen species defenses. We show that inhibiting both DGAT1 and superoxide dismutase 1 profoundly suppress tumor growth through eliciting intolerable oxidative stress.
    MeSH term(s) Animals ; Diacylglycerol O-Acyltransferase/genetics ; Diacylglycerol O-Acyltransferase/metabolism ; Melanoma ; Oncogene Proteins/metabolism ; Oxidative Stress ; Reactive Oxygen Species ; Triglycerides ; Zebrafish/metabolism
    Chemical Substances Oncogene Proteins ; Reactive Oxygen Species ; Triglycerides ; Diacylglycerol O-Acyltransferase (EC 2.3.1.20)
    Language English
    Publishing date 2024-02-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110995
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Spatially resolved phosphoproteomics reveals fibroblast growth factor receptor recycling-driven regulation of autophagy and survival.

    Watson, Joanne / Ferguson, Harriet R / Brady, Rosie M / Ferguson, Jennifer / Fullwood, Paul / Mo, Hanyi / Bexley, Katherine H / Knight, David / Howell, Gareth / Schwartz, Jean-Marc / Smith, Michael P / Francavilla, Chiara

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 6589

    Abstract: Receptor Tyrosine Kinase (RTK) endocytosis-dependent signalling drives cell proliferation and motility during development and adult homeostasis, but is dysregulated in diseases, including cancer. The recruitment of RTK signalling partners during ... ...

    Abstract Receptor Tyrosine Kinase (RTK) endocytosis-dependent signalling drives cell proliferation and motility during development and adult homeostasis, but is dysregulated in diseases, including cancer. The recruitment of RTK signalling partners during endocytosis, specifically during recycling to the plasma membrane, is still unknown. Focusing on Fibroblast Growth Factor Receptor 2b (FGFR2b) recycling, we reveal FGFR signalling partners proximal to recycling endosomes by developing a Spatially Resolved Phosphoproteomics (SRP) approach based on APEX2-driven biotinylation followed by phosphorylated peptides enrichment. Combining this with traditional phosphoproteomics, bioinformatics, and targeted assays, we uncover that FGFR2b stimulated by its recycling ligand FGF10 activates mTOR-dependent signalling and ULK1 at the recycling endosomes, leading to autophagy suppression and cell survival. This adds to the growing importance of RTK recycling in orchestrating cell fate and suggests a therapeutically targetable vulnerability in ligand-responsive cancer cells. Integrating SRP with other systems biology approaches provides a powerful tool to spatially resolve cellular signalling.
    MeSH term(s) Receptor, Fibroblast Growth Factor, Type 2/metabolism ; Ligands ; Endosomes/metabolism ; Endocytosis/physiology ; Autophagy ; Fibroblast Growth Factor 10/metabolism
    Chemical Substances Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1) ; Ligands ; Fibroblast Growth Factor 10
    Language English
    Publishing date 2022-11-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-34298-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Reciprocal priming between receptor tyrosine kinases at recycling endosomes orchestrates cellular signalling outputs.

    Smith, Michael P / Ferguson, Harriet R / Ferguson, Jennifer / Zindy, Egor / Kowalczyk, Katarzyna M / Kedward, Thomas / Bates, Christian / Parsons, Joseph / Watson, Joanne / Chandler, Sarah / Fullwood, Paul / Warwood, Stacey / Knight, David / Clarke, Robert B / Francavilla, Chiara

    The EMBO journal

    2021  Volume 40, Issue 14, Page(s) e107182

    Abstract: Integration of signalling downstream of individual receptor tyrosine kinases (RTKs) is crucial to fine-tune cellular homeostasis during development and in pathological conditions, including breast cancer. However, how signalling integration is regulated ... ...

    Abstract Integration of signalling downstream of individual receptor tyrosine kinases (RTKs) is crucial to fine-tune cellular homeostasis during development and in pathological conditions, including breast cancer. However, how signalling integration is regulated and whether the endocytic fate of single receptors controls such signalling integration remains poorly elucidated. Combining quantitative phosphoproteomics and targeted assays, we generated a detailed picture of recycling-dependent fibroblast growth factor (FGF) signalling in breast cancer cells, with a focus on distinct FGF receptors (FGFRs). We discovered reciprocal priming between FGFRs and epidermal growth factor (EGF) receptor (EGFR) that is coordinated at recycling endosomes. FGFR recycling ligands induce EGFR phosphorylation on threonine 693. This phosphorylation event alters both FGFR and EGFR trafficking and primes FGFR-mediated proliferation but not cell invasion. In turn, FGFR signalling primes EGF-mediated outputs via EGFR threonine 693 phosphorylation. This reciprocal priming between distinct families of RTKs from recycling endosomes exemplifies a novel signalling integration hub where recycling endosomes orchestrate cellular behaviour. Therefore, targeting reciprocal priming over individual receptors may improve personalized therapies in breast and other cancers.
    MeSH term(s) Cell Line, Tumor ; Endocytosis/physiology ; Endosomes/metabolism ; ErbB Receptors/metabolism ; Fibroblast Growth Factors/metabolism ; Humans ; Phosphorylation/physiology ; Protein Transport/physiology ; Signal Transduction/physiology ; Tyrosine/metabolism
    Chemical Substances Tyrosine (42HK56048U) ; Fibroblast Growth Factors (62031-54-3) ; ErbB Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2021-06-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.15252/embj.2020107182
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Differential responses to kinase inhibition in FGFR2-addicted triple negative breast cancer cells: a quantitative phosphoproteomics study.

    Cunningham, Debbie L / Sarhan, Adil R / Creese, Andrew J / Larkins, Katherine P B / Zhao, Hongyan / Ferguson, Harriet R / Brookes, Katie / Marusiak, Anna A / Cooper, Helen J / Heath, John K

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 7950

    Abstract: Fibroblast Growth Factor (FGF) dependent signalling is frequently activated in cancer by a variety of different mechanisms. However, the downstream signal transduction pathways involved are poorly characterised. Here a quantitative differential ... ...

    Abstract Fibroblast Growth Factor (FGF) dependent signalling is frequently activated in cancer by a variety of different mechanisms. However, the downstream signal transduction pathways involved are poorly characterised. Here a quantitative differential phosphoproteomics approach, SILAC, is applied to identify FGF-regulated phosphorylation events in two triple- negative breast tumour cell lines, MFM223 and SUM52, that exhibit amplified expression of FGF receptor 2 (FGFR2) and are dependent on continued FGFR2 signalling for cell viability. Comparative Gene Ontology proteome analysis revealed that SUM52 cells were enriched in proteins associated with cell metabolism and MFM223 cells enriched in proteins associated with cell adhesion and migration. FGFR2 inhibition by SU5402 impacts a significant fraction of the observed phosphoproteome of these cells. This study expands the known landscape of FGF signalling and identifies many new targets for functional investigation. FGF signalling pathways are found to be flexible in architecture as both shared, and divergent, responses to inhibition of FGFR2 kinase activity in the canonical RAF/MAPK/ERK/RSK and PI3K/AKT/PDK/mTOR/S6K pathways are identified. Inhibition of phosphorylation-dependent negative-feedback pathways is observed, defining mechanisms of intrinsic resistance to FGFR2 inhibition. These findings have implications for the therapeutic application of FGFR inhibitors as they identify both common and divergent responses in cells harbouring the same genetic lesion and pathways of drug resistance.
    MeSH term(s) Cell Line, Tumor ; Gene Ontology ; Humans ; Phosphoproteins/metabolism ; Protein Kinase Inhibitors/pharmacology ; Proteomics ; Receptor, Fibroblast Growth Factor, Type 2/antagonists & inhibitors ; Receptor, Fibroblast Growth Factor, Type 2/metabolism ; Triple Negative Breast Neoplasms/pathology
    Chemical Substances Phosphoproteins ; Protein Kinase Inhibitors ; Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1)
    Language English
    Publishing date 2020-05-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-64534-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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