Objective： To investigate the As4S4 induced growth inhibition and apoptosis in HeLa cells and its possible relationship with cyclooxygenase-2 （COX-2）. Methods： HeLa cells were treated with various concentrations ...
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Objective： To investigate the As4S4 induced growth inhibition and apoptosis in HeLa cells and its possible relationship with cyclooxygenase-2 （COX-2）. Methods： HeLa cells were treated with various concentrations （7.5, 15, 30, 60 mg/L） of As4S4 at different times （12, 24, 36, 48, 60 h）. Cell growth was measured by MTT. Apoptosis was detected by double staining flow cytometry （FCM）. Levels of PGE2 were measured by radioimmunoassay. The expression of COX-2 protein was examined by Western blot analysis. Results： After treated with different concentrations of As4S4, the growth of HeLa cells was suppressed significantly in a dose-and time-dependent manner. The IC50 of 24 h was 30 mg/L （P〈0.01）. As4S4 induced apoptosis with apoptosis rates at 8.13%-62.36% by flow cytometry （FCM） in a dose-dependent manners. The release of PGE2 was reduced in HeLa cells with the values being （70.56±2.03）, （48.58±2.28）, （29.25±1.57） and （18.02±1.04） respectively, significantly different compared with control group （3.15±0.01） （P〈0.01）. As4S4 also inhibited the activity and expression of COX-2 in a dose dependent manner and down-regulated the expression of COX-2 protein greatly. Conclusion： As4S4 could inhibit the proliferation and increase apoptosis in human HeLa cells. These effects may depend on the inhibition of the expression of COX-2 and PGE2 by As4S4.
To investigate the relationship between the expression of cyclooxygenase-2 （COX-2） and menstrual cycle, the regulatory effects of 17-β-estradiol （E2） and medroxyprogesterone acetate （MPA） on the expression of C...
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To investigate the relationship between the expression of cyclooxygenase-2 （COX-2） and menstrual cycle, the regulatory effects of 17-β-estradiol （E2） and medroxyprogesterone acetate （MPA） on the expression of COX-2 in cervical cancer Hela cells were examined. Cervical cancer specimens were obtained from 47 pre-menopausal patients. The phase of menstrual cycle was determined by case history and HE staining of uterine endometrium. COX-2 was immunohistochemically stained by SABC staining and the staining intensity was determined with computerized image analysis system. Hela cells were incubated with alcohol, E2, E2＋MPA, MPA for 12, 24 and 48 h respectively. The expression of COX-2 in Hela cells was detected by Western blotting and reverse transcriptase-polymerase chain reaction （RT-PCR）. Our results showed that the expression of COX-2 was significantly higher during proliferative phase than secretory phase （P〈0.05）, but there was no difference in the positive rate between proliferative phase and secretory phase （P〉0.05）. Incubation with E2 could significantly enhance the expression of COX-2 continually. On the contrary, E2＋MPA and MPA alone could decrease the expression of COX-2 as compared with the control and E2 group （P〈0.05 and P〈0.01 respectively）. It is concluded that the expression of COX-2 in cervical cancer of pre-menopausal patients and Hela cells was regulated by estrogen/progestogen.
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