4EGI-1 is a disruptor of the eIF4E/eIF4G interaction, with a binding dissociation constant (Kd) of 25 μM against eIF4E. It interferes with the eIF4F complex formation and reduces oncogenic protein expression in mammalian cells. Additionally, 4EGI-1, in concentrations up to 40 μM, displays proapoptotic activities and curtails the proliferation of various cancer cell lines[1]. 4EGI-1 shows cytotoxicity toward breast cancer cell lines like SKBR-3, MCF-7, and MDA-MB-231, achieving an approximate IC50 value of 30 μM. It is more potent against non-Cancer stem cells (CSCs) with an IC50 around 22 μM. At 40 μM, 4EGI-1 facilitates the differentiation of breast CSCs and at 8 μM, it prevents the formation of tube-like structures in HUVEC cells induced by breast CSCs. 4EGI-1 is also noted for selectively targeting translation processes important for CSC maintenance and spread[2]. In U87 cells, 4EGI-1 at 50 μM inhibits the assembly of the eIF4F complex. It suppresses cell proliferation and promotes apoptosis at concentrations of 10, 50, and 100 μM through Bax activation. Furthermore, 4EGI-1 induces mitochondrial dysfunction and triggers endoplasmic reticulum stress by activating GRP-78 in U87 cells[3].
体内研究
In vivo, 4EGI-1 administered at 75 mg/kg intraperitoneally is effective in diminishing the growth and angiogenesis of breast cancer stem cell tumors[2].
Additionally, the same dosage (75 mg/kg, i.p.) demonstrates a significant reduction in tumor volume and weight in mice implanted with U87 cells[3].
体外研究
4EGI-1 is a disruptor of the eIF4E/eIF4G interaction, with a binding dissociation constant (Kd) of 25 μM against eIF4E. It interferes with the eIF4F complex formation and reduces oncogenic protein expression in mammalian cells. Additionally, 4EGI-1, in concentrations up to 40 μM, displays proapoptotic activities and curtails the proliferation of various cancer cell lines[1].
4EGI-1 shows cytotoxicity toward breast cancer cell lines like SKBR-3, MCF-7, and MDA-MB-231, achieving an approximate IC50 value of 30 μM. It is more potent against non-Cancer stem cells (CSCs) with an IC50 around 22 μM. At 40 μM, 4EGI-1 facilitates the differentiation of breast CSCs and at 8 μM, it prevents the formation of tube-like structures in HUVEC cells induced by breast CSCs. 4EGI-1 is also noted for selectively targeting translation processes important for CSC maintenance and spread[2].
In U87 cells, 4EGI-1 at 50 μM inhibits the assembly of the eIF4F complex. It suppresses cell proliferation and promotes apoptosis at concentrations of 10, 50, and 100 μM through Bax activation. Furthermore, 4EGI-1 induces mitochondrial dysfunction and triggers endoplasmic reticulum stress by activating GRP-78 in U87 cells[3].
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