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Dual Role of p73 in Cancer Microenvironment and DNA Damage Response.
Rozenberg, Julian M; Zvereva, Svetlana; Dalina, Alexandra; Blatov, Igor; Zubarev, Ilya; Luppov, Daniil; Bessmertnyi, Alexander; Romanishin, Alexander; Alsoulaiman, Lamak; Kumeiko, Vadim; Kagansky, Alexander; Melino, Gerry; Barlev, Nikolai A.
Afiliação
  • Rozenberg JM; Laboratory of Cell Signaling Regulation, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia.
  • Zvereva S; Laboratory of Cell Signaling Regulation, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia.
  • Dalina A; The Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
  • Blatov I; Laboratory of Cell Signaling Regulation, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia.
  • Zubarev I; Laboratory of Cell Signaling Regulation, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia.
  • Luppov D; Laboratory of Cell Signaling Regulation, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia.
  • Bessmertnyi A; Faculty of Computer Science, School of Software Engineering, Higher School of Economics University, 101000 Moscow, Russia.
  • Romanishin A; School of Life Sciences, Immanuel Kant Baltic Federal University, 236041 Kaliningrad, Russia.
  • Alsoulaiman L; School of Biomedicine, Far Eastern Federal University, 690091 Vladivostok, Russia.
  • Kumeiko V; Laboratory of Cell Signaling Regulation, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia.
  • Kagansky A; School of Biomedicine, Far Eastern Federal University, 690091 Vladivostok, Russia.
  • Melino G; Laboratory of Cell Signaling Regulation, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia.
  • Barlev NA; School of Biomedicine, Far Eastern Federal University, 690091 Vladivostok, Russia.
Cells ; 10(12)2021 12 13.
Article em En | MEDLINE | ID: mdl-34944027
Understanding the mechanisms that regulate cancer progression is pivotal for the development of new therapies. Although p53 is mutated in half of human cancers, its family member p73 is not. At the same time, isoforms of p73 are often overexpressed in cancers and p73 can overtake many p53 functions to kill abnormal cells. According to the latest studies, while p73 represses epithelial-mesenchymal transition and metastasis, it can also promote tumour growth by modulating crosstalk between cancer and immune cells in the tumor microenvironment, M2 macrophage polarisation, Th2 T-cell differentiation, and angiogenesis. Thus, p73 likely plays a dual role as a tumor suppressor by regulating apoptosis in response to genotoxic stress or as an oncoprotein by promoting the immunosuppressive environment and immune cell differentiation.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteína Supressora de Tumor p53 / Carcinogênese / Proteína Tumoral p73 / Neoplasias Limite: Humans Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteína Supressora de Tumor p53 / Carcinogênese / Proteína Tumoral p73 / Neoplasias Limite: Humans Idioma: En Ano de publicação: 2021 Tipo de documento: Article