Oncogenic signaling of MEK5-ERK5.

Hoang, Van T; Yan, Thomas J; Cavanaugh, Jane E; Flaherty, Patrick T; Beckman, Barbara S; Burow, Matthew E

Hoang, Van T; Yan, Thomas J; Cavanaugh, Jane E; Flaherty, Patrick T; Beckman, Barbara S; Burow, Matthew E.

Afiliação

Hoang VT; Department of Medicine-Section of Hematology and Medical Oncology, Tulane University, New Orleans, LA, USA.
Yan TJ; Department of Medicine-Section of Hematology and Medical Oncology, Tulane University, New Orleans, LA, USA.
Cavanaugh JE; Department of Pharmacological Sciences, Division of Medicinal Chemistry, Mylan School of Pharmacy, Duquesne University, Pittsburgh, PA, USA.
Flaherty PT; Department of Pharmacological Sciences, Division of Medicinal Chemistry, Mylan School of Pharmacy, Duquesne University, Pittsburgh, PA, USA.
Beckman BS; Department of Pharmacology, Tulane University, New Orleans, LA, USA.
Burow ME; Department of Medicine-Section of Hematology and Medical Oncology, Tulane University, New Orleans, LA, USA; Department of Pharmacology, Tulane University, New Orleans, LA, USA; Tulane Cancer Center, Tulane University, New Orleans, LA, USA. Electronic address: mburow@tulane.edu.

Cancer Lett ; 392: 51-59, 2017 04 28.

Article em En | MEDLINE | ID: mdl-28153789

ABSTRACT

ABSTRACT

Mitogen-activated protein kinases (MAPKs) regulate diverse cellular processes including proliferation, cell survival, differentiation, and apoptosis. While conventional MAPK constituents have well-defined roles in oncogenesis, the MEK5 pathway has only recently emerged in cancer research. In this review, we consider the MEK5 signaling cascade, focusing specifically on its involvement in drug resistance and regulation of aggressive cancer phenotypes. Moreover, we explore the role of MEK5/ERK5 in tumorigenesis and metastatic progression, discussing the discrepancies in preclinical studies and assessing its viability as a therapeutic target for anti-cancer agents.

Assuntos

MAP Quinase Quinase 5/metabolismo; Proteína Quinase 7 Ativada por Mitógeno/metabolismo; Neoplasias/metabolismo; Proteínas Proto-Oncogênicas/metabolismo; Transdução de Sinais; Animais; Antineoplásicos/uso terapêutico; Apoptose; Diferenciação Celular; Proliferação de Células; Resistencia a Medicamentos Antineoplásicos; Humanos; MAP Quinase Quinase 5/antagonistas & inibidores; MAP Quinase Quinase 5/genética; Terapia de Alvo Molecular; Mutação; Neoplasias/tratamento farmacológico; Neoplasias/genética; Neoplasias/patologia; Inibidores de Proteínas Quinases/uso terapêutico; Proteínas Proto-Oncogênicas/genética; Transdução de Sinais/efeitos dos fármacos

Palavras-chave

Cellular signaling; Kinase inhibitors; MEK5-ERK5; Mitogen-activated protein kinase; Targeted therapies

Texto completo

Imprimir

XML

PubMed Links

Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Proteínas Proto-Oncogênicas / MAP Quinase Quinase 5 / Proteína Quinase 7 Ativada por Mitógeno / Neoplasias Limite: Animals / Humans Idioma: En Revista: Cancer Lett Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Estados Unidos

Texto completo

Imprimir

XML

PubMed Links

Buscar no Google