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- Title
Er-α 36 Affects the Migration, Invasion and Proliferation of Cervical Cancer Cells through MAPK/ERK Signaling Pathway Stimulated by Estrogen.
- Authors
Sijun Liu; Qin Peng
- 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.
- Subjects
ESTROGEN; ESTROGEN receptors; CERVICAL cancer; CELL lines; CELL proliferation
- Publication
Acta Microscopica, 2020, Vol 29, Issue 4, p2044
- ISSN
0798-4545
- Publication type
Article