The Effect Of Nicotine On The Cell Proliferation And The Expression Of Estrogen And Progesterone Receptor Of Endometrial Carcinoma Cell Line Ishikawa

Background and ObjectiveEndometrial carcinoma is one of the three most common gynecological cancer. In recent years, due to humankind’s increasing longevity and widespread use of exogenous estrogen, its incedence is on the rise at home and abroad. The etiology of endometrial carcinoma is unclear, but it is likely to associate with the long-term effects of estrogen. Recent epidemiological survey showed that the onset risk of endometrial cancer can decreased in the women who have a smoke. Most researchers think that it is related to the anti-estrogen effect of nicotine, but the mechanism is still unclear. At the same time, due to the phenomena of progesterone resistance, more and more researchers are interested in the influence of nicotine on progesterone, which still needs more research to clear. This research is about the effect of nicotine on the cell proliferation and the expression of estrogen and progesterone receptor of endometrial carcinoma cell line Ishikawa, which will help us understand the mechanism further, and bring new ideas into the prevention and therapy of endometrial carcinoma.MethodsThis research has two parts:in the first part, the Ishikawa cells were treated with different concentrations of nicotine, β-estradiol, and nicotine-estradiol for0,24,48,72hours, respectively. Then, the proliferation of the cells were measured by CCK8methods. In the second part, the Ishikawa cells were treated with different concentrations of nicotine,β-estradiol, and nicotine-estradiol for24hours, respectively. The percentage of labled cells were observed by flow cytometry after immunofluorescence staining with anti-ER and anti-PR.Results In the first part, it was not found that nicotine can affect the proliferation of Ishikawa cells(p>0.05), and P-estradiol can promote the proliferation of Ishikawa cells(p<0.05). The effect of P-estradiol can be inhibited by nicotine, which a obvious statistical significance was showm(p<0.05). In the second part, nicotine and β-estradiol can decrease the percentage of ER-labled cells of Ishikawa (P<0.05) However there is no statistical difference between different groups (P>0.05).10-8M β-estradiol and10M nicotine can decrease the percentage of ER-labled cells compared to control group (P<0.05), but increase the percentage of ER-labled cells compared to nicotine groups and P-estradiol group (P<0.05).10-3M nicotine can increase the the percentage of PR-labled cells of Ishikawa (P<0.05). However,10-4M、10-5M nicotine can decrease the the percentage of PR-labled cells (P<0.05).10-8M β-estradiol and10-4M nicotine can decrease the percentage of PR-labled cells compared to P-estradiol group (P<0.05), but increase the percentage of PR-labled cells compared to10-4M nicotine group.ConclusionsNicotine can not inhibite the proliferation of the cells of endometrial carcinoma directly, but it displays a strong antagonism for the effect of promoting cell proliferation of β-estradiol. Nicotine can inhibite the expression of ER. The higher concentration of nicotine can increase the expression of PR, but the lower concentration can decrease the expression of PR.