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The complementary roles of STAT3 and STAT1 in cancer biology: insights into tumor pathogenesis and therapeutic strategies
被引:21
|作者:
Wang, Weiyuan
[1
]
McDonald, Melanie Cristina Lopez
[1
]
Kim, Christine
[1
]
Ma, Mirielle
[1
]
Pan, Zetao
[1
]
Kaufmann, Charlotte
[1
]
Frank, David A.
[1
]
机构:
[1] Emory Univ, Winship Canc Inst, Dept Hematol & Med Oncol, Sch Med, Atlanta, GA 30307 USA
来源:
关键词:
cancer;
oncology;
transcription factors;
signal transduction;
tumor immunology;
protein phosphorylation;
RECEPTOR SIGNALING PATHWAYS;
IFN-GAMMA;
CONSTITUTIVE ACTIVATION;
INTERFERON-GAMMA;
JAK-STAT;
IMMUNE-RESPONSES;
GROWTH-FACTOR;
CELLS;
GENE;
TRANSCRIPTION;
D O I:
10.3389/fimmu.2023.1265818
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
STATs are a family of transcription factors that regulate many critical cellular processes such as proliferation, apoptosis, and differentiation. Dysregulation of STATs is frequently observed in tumors and can directly drive cancer pathogenesis. STAT1 and STAT3 are generally viewed as mediating opposite roles in cancer development, with STAT1 suppressing tumorigenesis and STAT3 promoting oncogenesis. In this review, we investigate the specific roles of STAT1 and STAT3 in normal physiology and cancer biology, explore their interactions with each other, and offer insights into therapeutic strategies through modulating their transcriptional activity.
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页数:12
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