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. 2018 Sep 12;23(9):2334. doi: 10.3390/molecules23092334

Figure 1.

Figure 1

Molecular mechanisms of (-)-epigallocatechingallate (EGCG) suppressing the proliferation of cervical cancer cells. EGCG down-regulated the expressions of E6, E7, EGFR, IGF-1 and HIF-1, then the expressions of downstream targets such as the AKT/PI3K pathway, mTOR pathway and ERK1/2 also declined. The decline of E6 could up-regulated P53 expression resulting in P21 and P27 up-regulations, then CDK2 was down-regulated. The down-regulation of the mTOR pathway led to VEGF reduction. Eventually, the reduced expressions of ERK1/2, VEGF and CDK2 suppressed the proliferation of cervical cancer cells (broken lines mean indirect approaches). AKT: protein kinase B; CDK2: cyclin-dependent kinase 2; E6: one of human papillomavirus (HPV) oncogenes; E7: another HPV oncogene; EGFR: epidermal growth factor receptor; ERK: extracellular signal-regulated kinase; HIF-1: hypoxia-inducible factor 1; IGF-1: insulin-like growth factor 1; mTOR: mammalian target of rapamycin; P21: tumor suppressor protein; P27: tumor suppressor protein; P53: tumor suppressor protein; PI3K: phosphoinositide-3-kinase; VEGF: vascular endothelial growth factor.