Figure 7.

The classic mechanism for E2 action is E2 diffusing into the nucleus, binding to the nucleus estrogen receptor (ER), combining with ERE on DNA, starting transcription translation and inducing the cycle of multiplication in cancer cells. In addition, activated ERα can activate AP-1 and SP-1, which are transcription enhancers that can promote the transcription translation of ERE and enable incomplete ERE (half ERE) to transcribe and translate. SSCE may affect the activation of ERα, decreasing p-ERα, reducing the combination ability of ER and ERE, and stopping ERE from transcribing and translating. On the other hand, E2 can combine with GPER on the cell membrane, increase the expression of ERK, promote cell proliferation, activate the PI3K-AKT pathway, increase the activation of mTOR and the upregulation of Bcl-2 and cyclin D, downregulate Bax, reduce apoptosis, and start the cell cycle. Both ERK and AKT can inhibit JNK, reducing apoptosis. SSCE may downregulate the PI3K-AKT, ERK pathway by GPER, resulting in a downregulation of Bcl-2, upregulation of Bax, reduction in the inhibition of JNK, promotion of cell apoptosis, and downregulation of cyclin D, thereby blocking the cell cycle.