scholarly journals Regulation of endometrial cancer cell growth by luteinizing hormone (LH) and follicle stimulating hormone (FSH)

2000 ◽  
Vol 83 (12) ◽  
pp. 1730-1734 ◽  
Author(s):  
S Davies ◽  
C M R Bax ◽  
E Chatzaki ◽  
T Chard ◽  
R K Iles
Keyword(s):  
Endometrial Cancer ◽  
Cell Growth ◽  
Luteinizing Hormone ◽  
Cancer Cell ◽  
Follicle Stimulating Hormone ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Stimulating Hormone

scholarly journals Restoration of microRNA‑29c in type I endometrioid cancer reduced endometrial cancer cell growth

2019 ◽  
Author(s):  
Michelle Van Sinderen ◽  
Meaghan Griffiths ◽  
Ellen Menkhorst ◽  
Keith Niven ◽  
Evdokia Dimitriadis
Keyword(s):  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Type I ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell

Inhibition of human endometrial cancer cell growth in vitro and in vivo by somatostatin analog RC-160

1999 ◽  
Vol 181 (3) ◽  
pp. 583-590 ◽  
Author(s):  
Misako Mishima ◽  
Tetsu Yano ◽  
Haruko Jimbo ◽  
Naomi Yano ◽  
Yutaka Morita ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Somatostatin Analog ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell

scholarly journals Protein kinase C alpha-dependent signaling mediates endometrial cancer cell growth and tumorigenesis

2009 ◽  
Vol 125 (11) ◽  
pp. 2556-2564 ◽  
Author(s):  
James M. Haughian ◽  
Elaine M. Reno ◽  
Alicia M. Thorne ◽  
Andrew P. Bradford
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Kinase C ◽  
Protein Kinase C Alpha

scholarly journals Retinoic acid inhibits endometrial cancer cell growth via multiple genomic mechanisms

2011 ◽  
Vol 46 (2) ◽  
pp. 139-153 ◽  
Author(s):  
Y.-H. Cheng ◽  
H. Utsunomiya ◽  
M. E. Pavone ◽  
P. Yin ◽  
S. E. Bulun
Keyword(s):  
Endometrial Cancer ◽  
Retinoic Acid ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell

scholarly journals Metapristone (RU486 derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

2020 ◽  
Author(s):  
Yue Chang ◽  
Min Hao ◽  
Ru Jia ◽  
Yihui Zhao ◽  
Yixuan Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Downstream Target ◽  
Ishikawa Cells

Abstract Background: Endometrial cancer is one of the most common cancers affecting women's health. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Recent studies have reported that endometrial cancer is also related with the sexual-mediated hormones. The purpose of this research is to treat the endometrial cancer with the hormone-related drugs, and find out the specific molecular mechanism. Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. The protein expression was measured by western blot. Cell proliferation was monitored using the MTT assay and cell colony formation assay. Cell apoptosis was monitored using EdU assay. Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1. Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.

scholarly journals Metapristone (RU486 derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

2020 ◽  
Author(s):  
Yue Chang ◽  
Min Hao ◽  
Ru Jia ◽  
Yihui Zhao ◽  
Yixuan Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Downstream Target ◽  
Ishikawa Cells

Abstract Background: Endometrial cancer is the prevalent invasive gynecological cancer in the world. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Metapristone is a hormone related drug and widely used in endometrial cancer clinical therapeutics. However, the deep regulatory mechanism of metapristone is not clear. In this research, we aimed to figure out the specific molecular mechanism during the treatment of endometrial cancer with metapristone.Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. Moreover, the mice tumor model was used to confirm the function of metapristone and the regulating process by miR-492/Klf5/Nrf1 axis in vivo. The protein expression was measured by western blot. Cell proliferation and apoptosis was monitored using the MTT assay, cell colony formation assay and EdU assay.Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1. Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.

scholarly journals Metapristone (RU486-derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

2020 ◽  
Author(s):  
Yue Chang ◽  
Min Hao ◽  
Ru Jia ◽  
Yihui Zhao ◽  
Yixuan Cai ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Downstream Target

Abstract Background: Endometrial cancer is an invasive gynecological cancer prevalent in the world. The pathogenesis of endometrial cancer is related to multiple levels of regulation, referring to oestrogen, tumor-suppressor gene (e.g. PTEN ) or microRNAs (e.g. miR-23a and miR-29b). Metapristone is a hormone-related drug, which is widely used in clinical treatment of endometrial cancer. However, the underlying regulatory mechanism of metapristone on endometrial cancer is still unclear, especially the regulatory effect on microRNAs. The aim of this study is to investigate the specific molecular mechanism of metapristone regulating microRNAs in the treatment of endometrial cancer. Methods: RL95-2 cells and Ishikawa cells were used as the endometrial cancer models. MiR-492 or si-miR-492 was transfected into RL95-2 cells and Ishikawa cells to explore the role of miR-492 in endometrial cancer. The cell cancer model and mice cancer model were used to confirm the function and mechanism of metapristone affected on endometrial cancer in vitro and in vivo . Mechanically, cell proliferation was monitored using the MTT assay, cell colony formation assay and EdU assay. Luciferase reporter assay was used to identify the downstream target gene of miR492. The protein expression and RNA expression were respectively measured by western blot and qRT-PCR for cell signaling pathway research, subsequently, were verified in the mice tumor model via immunohistochemistry. Results: Metapristone as a kind of hormone-related drug significantly inhibited the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Mechanically, miR-492 and its target genes Klf5 and Nrf1 were highly expressed in the endometrial cancer cell lines, which promoted cell proliferation and inhibited cell apoptosis. Metapristone decreased the expression of miR-492 and its target genes Klf5 and Nrf1 , leading to endometrial cancer cell growth inhibition in vitro and in vivo . Conclusion: Metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis-related signaling pathway and decreasing the expression of miR-492 and its downstream target genes ( Klf5 and Nrf1 ), which provided the theoretical basis in clinical treatment of endometrial cancer.

scholarly journals Metapristone (RU486-derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yue Chang ◽  
Min Hao ◽  
Ru Jia ◽  
Yihui Zhao ◽  
Yixuan Cai ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Downstream Target

Abstract Background Endometrial cancer is an invasive gynecological cancer prevalent in the world. The pathogenesis of endometrial cancer is related to multiple levels of regulation, referring to oestrogen, tumor-suppressor gene (e.g. PTEN) or microRNAs (e.g. miR-23a and miR-29b). Metapristone is a hormone-related drug, which is widely used in clinical treatment of endometrial cancer. However, the underlying regulatory mechanism of metapristone on endometrial cancer is still unclear, especially the regulatory effect on microRNAs. The aim of this study is to investigate the specific molecular mechanism of metapristone regulating microRNAs in the treatment of endometrial cancer. Methods RL95-2 cells and Ishikawa cells were used as the endometrial cancer models. MiR-492 or si-miR-492 was transfected into RL95-2 cells and Ishikawa cells to explore the role of miR-492 in endometrial cancer. The cell cancer model and mice cancer model were used to confirm the function and mechanism of metapristone affected on endometrial cancer in vitro and in vivo. Mechanically, cell proliferation was monitored using MTT assay, cell colony formation assay and EdU assay. Luciferase reporter assay was used to identify the downstream target gene of miR-492. The protein expression and RNA expression were respectively measured by western blot and qRT-PCR for cell signaling pathway research, subsequently, were verified in the mice tumor model via immunohistochemistry. Results Metapristone as a kind of hormone-related drug significantly inhibited the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Mechanically, miR-492 and its target genes Klf5 and Nrf1 were highly expressed in the endometrial cancer cell lines, which promoted cell proliferation and inhibited cell apoptosis. Metapristone decreased the expression of miR-492 and its target genes Klf5 and Nrf1, leading to endometrial cancer cell growth inhibition in vitro and in vivo. Conclusion Metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis-related signaling pathway and decreasing the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis in clinical treatment of endometrial cancer.

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