scholarly journals Cellular mechanisms of growth inhibition of human endometrial cancer cell line by an antagonist of growth hormone-releasing hormone

2008 ◽  
Author(s):  
Lin Zhao ◽  
Tetsu Yano ◽  
Yutaka Osuga ◽  
Shunsuke Nakagawa ◽  
Hajime Oishi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Endometrial Cancer ◽  
Growth Inhibition ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Growth Hormone Releasing Hormone ◽  
Cellular Mechanisms ◽  
Endometrial Cancer Cell ◽  
Releasing Hormone

Growth inhibition by danazol in a human endometrial cancer cell line with estrogen-independent progesterone receptors

1987 ◽  
Vol 28 (5) ◽  
pp. 571-574 ◽  
Author(s):  
Naoki Terakawa ◽  
Hiromasa Ikegami ◽  
Ikuya Shimizu ◽  
Toshihiro Aono ◽  
Osamu Tanizawa ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Growth Inhibition ◽  
Cell Line ◽  
Cancer Cell ◽  
Progesterone Receptors ◽  
Cancer Cell Line ◽  
Endometrial Cancer Cell

Effects of Sex Steroid Hormones on Corticosteroid-Binding Globulin Gene Expression in Human Endometrial Cancer Cell Line Ishikawa

1998 ◽  
Vol 35 (5) ◽  
pp. 637-642 ◽  
Author(s):  
Ryou Misao ◽  
Yoshihito Nakanishi ◽  
Jiro Fujimoto ◽  
Teruhiko Tamaya
Keyword(s):  
Endometrial Cancer ◽  
Mrna Expression ◽  
Cell Line ◽  
Cancer Cell ◽  
Biological Effects ◽  
Cancer Cell Line ◽  
High Dose ◽  
Dependent Manner ◽  
Endometrial Cancer Cell ◽  
Corticosteroid Binding Globulin

The effect of progestins on intracellular corticosteroid-binding globulin (CBG) mRNA expression in an endometrial cancer cell line (Ishikawa) was examined in an attempt to understand the biological effects of high-dose progestins in the treatment of well-differentiated uterine endometrial cancers. Oestradiol-17β (E2) significantly increased CBG mRNA expression in a dose-dependent manner, while a high dose of progesterone with or without E2 suppressed it significantly. Furthermore, a high dose of progesterone or medroxyprogesterone acetate (MPA) suppressed CBG mRNA expression to a greater degree than did chlormadinone acetate or 17 α-hydroxyprogesterone caproate with or without E2. These findings suggest that the effects of high-dose progestins on cancer cells may be mediated via suppression of intracellular CBG.

scholarly journals Preclinical Efficacy and Involvement of AKT, mTOR, and ERK Kinases in the Mechanism of Sulforaphane against Endometrial Cancer

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1273 ◽  
Author(s):  
Rajani Rai ◽  
Kathleen Gong Essel ◽  
Doris Mangiaracina Benbrook ◽  
Justin Garland ◽  
Yan Daniel Zhao ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
M Cell ◽  
Vimentin Expression ◽  
Western Blots ◽  
Endometrial Cancer Cell ◽  
Mesenchymal Transition

Sulforaphane exerts anti-cancer activity against multiple cancer types. Our objective was to evaluate utility of sulforaphane for endometrial cancer therapy. Sulforaphane reduced viability of endometrial cancer cell lines in association with the G2/M cell cycle arrest and cell division cycle protein 2 (Cdc2) phosphorylation, and intrinsic apoptosis. Inhibition of anchorage-independent growth, invasion, and migration of the cell lines was associated with sulforaphane-induced alterations in epithelial-to-mesenchymal transition (EMT) markers of increased E-cadherin and decreased N-cadherin and vimentin expression. Proteomic analysis identified alterations in AKT, mTOR, and ERK kinases in the networks of sulforaphane effects in the Ishikawa endometrial cancer cell line. Western blots confirmed sulforaphane inhibition of AKT, mTOR, and induction of ERK with alterations in downstream signaling. AKT and mTOR inhibitors reduced endometrial cancer cell line viability and prevented further reduction by sulforaphane. Accumulation of nuclear phosphorylated ERK was associated with reduced sensitivity to the ERK inhibitor and its interference with sulforaphane activity. Sulforaphane induced apoptosis-associated growth inhibition of Ishikawa xenograft tumors to a greater extent than paclitaxel, with no evidence of toxicity. These results verify sulforaphane’s potential as a non-toxic treatment candidate for endometrial cancer and identify AKT, mTOR, and ERK kinases in the mechanism of action with interference in the mechanism by nuclear phosphorylated ERK.

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