Abstract
Early growth response factor 1 (EGR1) is a transcription factor that is mainly involved in the processes of tissue injury, immune responses, and fibrosis. Recent studies have shown that EGR1 is closely related to the initiation and progression of cancer and may participate in tumor cell proliferation, invasion, and metastasis and in tumor angiogenesis. Nonetheless, the specific mechanism whereby EGR1 modulates these processes remains to be elucidated. This review article summarizes possible mechanisms of action of EGR1 in tumorigenesis and tumor progression and may serve as a reference for clinical efficacy predictions and for the discovery of new therapeutic targets.
Highlights
Growth response factor 1 (EGR1) is a member of the EGR family and is known as EGR-1, NEFI-A, Zif268, Krox-24, and TIS85
A variety of MAPK pathways, such as ERK1 and -2, JNK, and p38 kinase cascades, participate in the expression of matrix metalloproteinase 1 (MMP1) caused by tumor necrosis factor alpha (TNF-a) by upregulating Early growth response factor 1 (EGR1) and promote tumor invasion and metastasis [39]
Tourtellotte et al showed that EGR4 loss upregulated EGR1 and slightly altered EGR2 and EGR3 [95]
Summary
Growth response factor 1 (EGR1) is a member of the EGR family and is known as EGR-1, NEFI-A, Zif268, Krox-24, and TIS85. CXCL5 ( known as ENA78) enhances EGR1 transcription via the RAF–MEK–ERK pathway, increasing SNAIL expression, tumor cell metastasis, and EMT [28]. EGR1 induced by hepatocyte growth factor (HGF) can directly bind to the promoter region of SNAIL, increase its expression, and lead to tumor cell metastasis [37].
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