The inhibitory effect of medroxyprogesterone acetate on steroid sulfatase in human uterine endometrial cancer cells

1996 ◽  
Vol 3 (4) ◽  
pp. 337-340 ◽  
Author(s):  
T Yamamoto ◽  
K Yokota ◽  
M Urabe ◽  
J Kitawaki ◽  
H Honjo
Author(s):  
Minglin Liang ◽  
Hui Chen ◽  
Jie Min

Endometrial cancer is a common gynecological malignancy, and the incidence of this disease has increased in recent years. Recently, some studies suggested that the expression of miR-379-5p suppressed the metastasis of breast cancer cells. However, whether the expression of miR-379-5p could affect the proliferation, migration and invasion of endometrial cancer is unclear. In this study, we established miR-379-5p overexpression and miR-379-5p inhibition in endometrial cancer cells. Next, EdU and colony formation assays were performed to measure proliferation of endometrial cancer cells. Wound healing and transwell assays were carried out to examine the migration and invasion of these cells. Then, luciferase reporter assay was performed to test the relationship between miR-379-5p and ROR1. Finally, we overexpressed ROR1 in miR-379-5p overexpressing endometrial cancer cells. Colony formation, wound healing and transwell assays were used to measure proliferation, migration and invasion of these cells. The results showed that overexpression of miR-379-5p repressed proliferation, migration and invasion of endometrial cancer cells. Higher levels of miR-379-5p repressed expression of N-cadherin, Vimentin and ZEB1. Overexpression of miR-379-5p also promoted expression of E-cadherin and ZO-1. In addition, miR-379-5p targeted and suppressed expression of ROR1. Overexpression of ROR1 abolished the inhibitory effect of miR-379-5p on proliferation, migration, invasion and EMT of endometrial cancer cells. All of these results indicated that miR-379-5p suppressed proliferation, migration and invasion of endometrial cancer cells by inhibiting the expression of ROR1 and the EMT process.


2011 ◽  
Vol 21 (2) ◽  
pp. 213-221 ◽  
Author(s):  
Zhenbo Zhang ◽  
Lingling Dong ◽  
Long Sui ◽  
Yixia Yang ◽  
Xuelian Liu ◽  
...  

Introduction:A long-term treatment with progestin commonly results in progestin resistance in endometrial cancer. So, the aim of this study was to investigate the role of glyoxalase I (GloI), a mediator of chemotherapy resistance, in metformin reversal of progestin resistance in endometrial carcinoma.Methods:The proliferation variety of endometrial cancer cells was determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-Diphenyltetrazolium (MTT) assay after exposure to medroxyprogesterone acetate, metformin, or both reagents; apoptosis rates were assessed by flow cytometry. Real-time polymerase chain reaction was used to evaluate the effect of small interfering RNA sequence on target gene expression. Western immunoblotting was performed to determine the expression of GloI and the molecules of the mammalian target of rapamycin (mTOR) pathway.Result:Knocking down GloI sensitized progestin-resistant Ishikawa cells to progestin. Metformin downregulated GloI expression, reversed progestin resistance, enhanced progestin-induced cell proliferation inhibition, and induced apoptosis in progestin-resistant Ishikawa cells. In addition, medroxyprogesterone acetate-induced mTOR phosphorylation was blocked by metformin. Metformin abolishes mTOR phosphorylation and inhibits GloI expression, attenuating proliferation and inducing apoptosis in progestin-resistant Ishikawa cells.Conclusions:Dysregulation of GloI expression in endometrial cancer may be part of the molecular mechanisms for progestin resistance.


1992 ◽  
Vol 167 (1) ◽  
pp. 207-211 ◽  
Author(s):  
Hiroaki Jikihara ◽  
Nobuyuki Terada ◽  
Reiko Yamamoto ◽  
Yoshinobu Nishikawa ◽  
Osamu Tanizawa ◽  
...  

Cancer ◽  
1984 ◽  
Vol 54 (6) ◽  
pp. 999-1001 ◽  
Author(s):  
Hans Huber ◽  
Peter Husslein ◽  
Werner Michalica ◽  
Peter Wagenbichler

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