Er-α 36 Affects the Migration, Invasion and Proliferation of Cervical Cancer Cells through MAPK/ERK Signaling Pathway Stimulated by Estrogen

  • Sijun Liu
Keywords: ER-α 36, cervical cancer, MAPK/ERK Signaling Pathway

Abstract

To investigate the effect of estrogen and estrogen receptor 36 (ER-α 36) on the migration, invasion and
proliferation of cervical cancer cells through mitogen activated protein kinase (MAPK)/extracellular signal
regulated kinase (ERK) signaling pathway stimulated by estrogen. The cervical cancer cell lines caskl and HeLa
were collected and divided into negative control group (untreated), low expression group (stable low expression
Er-α 36 cervical cancer cell line), high expression group (stable high expression Er-α 36 cervical cancer cell
line), estradiol (E2) group (E2 stimulated cervical cancer cell line), U0126 (MAPK activator inhibitor)+E2
group (The cervical cancer cell line was stimulated with E2 and treated with U0126. The number of cells
penetrating polycarbonate membrane, the ability of cell proliferation and the ability of cell migration were
compared among the negative control group, the low expression group and the high expression group. The
effects of estrogen on ERK1/2 phosphorylation and the degree of phosphorylation of ERK1/2 in the negative
control group, U0126+E2 group and e2erk1/2 were further analyzed. Compared with the negative control group,
the number of cells penetrating the polycarbonate membrane and the ability of proliferation in the low
expression group of Er-α 36 were significantly reduced, while the number of cells penetrating the polycarbonate
membrane and the ability of proliferation in the high expression group of Er-α 36 were significantly increased
(P<0.05). At 24h and 48h, compared with the negative control group, the cell migration ability of Er-α 36 low
expression group was significantly reduced (P<0.05). At 48h, compared with the negative control group, the cell
migration ability of Er-α 36 high expression group was significantly increased (P<0.05). At 24 hours, there was
no significant difference in cell migration between the two groups (P>0.05). ERK1/2 was rapidly
phosphorylated after estrogen treatment in two groups of cell lines, and the phosphorylation degree reached the
peak at 5-10 min, and the total amount of ERK1/2 did not change. Compared with the negative control group,
the phosphorylation level of ERK1/2 in U0126+E2 group decreased significantly, while that in E2 group
increased significantly (P<0.05). Conclusion: Er-α 36 can affect the migration, invasion and proliferation of
cervical cancer cells through MAPK/ERK signaling pathway stimulated by estrogen.

Published
2020-04-01