Signal transducer and activator of transcription 3 signaling in tumor immune evasion

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F22%3A50018287" target="_blank" >RIV/62690094:18470/22:50018287 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216305:26620/22:PU144087 RIV/62156489:43210/22:43920164

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/pii/S0163725821001716?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0163725821001716?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.pharmthera.2021.107969" target="_blank" >10.1016/j.pharmthera.2021.107969</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Signal transducer and activator of transcription 3 signaling in tumor immune evasion

Popis výsledku v původním jazyce

The underlying mechanism of tumor immune evasion is a highly concerning subject for researchers. Increasing evidences reveal that the over-activated signal transducer and activator of transcription 3 (STAT3) is a crucial molecular hub in malignant tumors. STAT3 controls autophagy molecules that impair CTL-mediated tumor cell lysis, inhibiting natural killer cells and inducing apoptosis in T lymphocytes to create an immunosuppressive environment. STAT3 signaling regulates the expression of immune factors and recruits immunosuppressive cells to establish a tolerant tumor microenvironment (TME). STAT3 signaling regulates the expression of immune factors and recruits immunosuppressive cells to create an immunosuppressive environment. All this aid tumor cells in escaping from immune surveillance. In this review, we outlined the STAT3-mediated mechanisms involved in tumor immune evasion and their potential regulatory functions in the TME. We discussed the impact of STAT3 signaling on PD-L1, HIF-1α, exosome, lncRNA, and autophagy in the promotion of tumor immune evasion and highlighted the recent research on STAT3 signaling and tumor immune evasion that may assist in developing effective STAT3-targeted drugs for advancing immunotherapy. © 2021 Elsevier Inc.

Název v anglickém jazyce

Signal transducer and activator of transcription 3 signaling in tumor immune evasion

Popis výsledku anglicky

The underlying mechanism of tumor immune evasion is a highly concerning subject for researchers. Increasing evidences reveal that the over-activated signal transducer and activator of transcription 3 (STAT3) is a crucial molecular hub in malignant tumors. STAT3 controls autophagy molecules that impair CTL-mediated tumor cell lysis, inhibiting natural killer cells and inducing apoptosis in T lymphocytes to create an immunosuppressive environment. STAT3 signaling regulates the expression of immune factors and recruits immunosuppressive cells to establish a tolerant tumor microenvironment (TME). STAT3 signaling regulates the expression of immune factors and recruits immunosuppressive cells to create an immunosuppressive environment. All this aid tumor cells in escaping from immune surveillance. In this review, we outlined the STAT3-mediated mechanisms involved in tumor immune evasion and their potential regulatory functions in the TME. We discussed the impact of STAT3 signaling on PD-L1, HIF-1α, exosome, lncRNA, and autophagy in the promotion of tumor immune evasion and highlighted the recent research on STAT3 signaling and tumor immune evasion that may assist in developing effective STAT3-targeted drugs for advancing immunotherapy. © 2021 Elsevier Inc.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30108 - Toxicology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2022

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Pharmacology and Therapeutics

ISSN

0163-7258

e-ISSN

1879-016X

Svazek periodika

230

Číslo periodika v rámci svazku

February

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

11

Strana od-do

"Article number: 107969"

Kód UT WoS článku

000764519900001

EID výsledku v databázi Scopus

2-s2.0-85114008413