Targeting Protein Kinase C in Glioblastoma Treatment

Autor: Geribaldi-Doldán, Noelia, Hervás-Corpión, Irati, Gómez-Oliva, Ricardo, Domínguez-García, Samuel, Ruiz, Félix A., Iglesias-Lozano, Irene, Carrascal, Livia, Pardillo-Díaz, Ricardo, Gil-Salú, José L., Nunez-Abades, Pedro, Valor, Luis M., Castro, Carmen
Přispěvatelé: [Geribaldi-Doldán,N, Pardillo-Díaz,R] Departamento de Anatomía y Embriología Humanas, Facultad de Medicina, Universidad de Cádiz, Cádiz, Spain. [Geribaldi-Doldán,N, Hervás-Corpión,I, Gómez-Oliva,R, Domínguez-García,S, Ruiz,FA, Iglesias-Lozano,I, Carrascal,L, Pardillo-Díaz,R, Gil-Salú,JL, Nunez-Abades,P, Valor,LM, Castro,C] Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Cádiz, Spain. [Hervás-Corpión,I, Valor,LM] Unidad de Investigación, Hospital Universitario Puerta del Mar de Cádiz, Cádiz, Spain. [Gómez-Oliva,R, Castro,C] Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, Cádiz, Spain. [Ruiz,FA] Área de Nutrición, Facultad de Medicina, Universidad de Cádiz, Cádiz, Spain. [Carrascal,L, Nunez-Abades,P] Departamento de Fisiología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain. [Valor,LM] Currently at Instituto de Investigación Sanitaria y Biomédica de Alicante (ISABIAL), Alicante, Spain, This research was co-financed by the Integrated Territorial Investment Operational Programme of the European Commission and by the Department of Department of Health and Families (Consejería de Salud y Familias) of the Regional Government of Andalusia. Project reference: ITI-0042-2019: ITI Cadiz 2019. L.M.V. is the recipient of a Miguel Servet II contract (CPII20/00025) financed by the Instituto de Salud Carlos III and Fondo Social Europeo 2014-2020, Programa Estatal de Promoción del Talento y su empleabilidad en I + D + i.
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Neurogénesis
Células madre
Neoplasias encefálicas
Diseases::Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Brain Neoplasms [Medical Subject Headings]
Neurogenesis
Ciclo celular
Apoptosis
Anatomy::Cells::Stem Cells::Neoplastic Stem Cells [Medical Subject Headings]
Cell cycle
Temozolomida
Enzastaurin
Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]
Neurregulinas
Protein kinase C
Temozolomide
Glioma stem cells
Neuregulin
Proteína quinasa C
Anatomy::Cells::Stem Cells::Neural Stem Cells [Medical Subject Headings]
Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Cycle [Medical Subject Headings]
Neural stem cells
Receptores ErbB
Epidermal growth factor receptor
Diseases::Neoplasms::Neoplasms by Histologic Type::Neoplasms
Germ Cell and Embryonal::Neuroectodermal Tumors::Neoplasms
Neuroepithelial::Glioma::Astrocytoma::Glioblastoma [Medical Subject Headings]

Células-madre neurales
Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]
Brain tumor
Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Isoenzymes [Medical Subject Headings]
Analytical
Diagnostic and Therapeutic Techniques and Equipment::Diagnosis::Prognosis [Medical Subject Headings]

Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Transferases::Phosphotransferases::Phosphotransferases (Alcohol Group Acceptor)::Protein Kinases::Protein-Serine-Threonine Kinases::Protein Kinase C [Medical Subject Headings]
Glioblastoma
Popis: Glioblastoma (GBM) is the most frequent and aggressive primary brain tumor and is associated with a poor prognosis. Despite the use of combined treatment approaches, recurrence is almost inevitable and survival longer than 14 or 15 months after diagnosis is low. It is therefore necessary to identify new therapeutic targets to fight GBM progression and recurrence. Some publications have pointed out the role of glioma stem cells (GSCs) as the origin of GBM. These cells, with characteristics of neural stem cells (NSC) present in physiological neurogenic niches, have been proposed as being responsible for the high resistance of GBM to current treatments such as temozolomide (TMZ). The protein Kinase C (PKC) family members play an essential role in transducing signals related with cell cycle entrance, differentiation and apoptosis in NSC and participate in distinct signaling cascades that determine NSC and GSC dynamics. Thus, PKC could be a suitable druggable target to treat recurrent GBM. Clinical trials have tested the efficacy of PKCβ inhibitors, and preclinical studies have focused on other PKC isozymes. Here, we discuss the idea that other PKC isozymes may also be involved in GBM progression and that the development of a new generation of effective drugs should consider the balance between the activation of different PKC subtypes. Yes
Databáze: OpenAIRE