scholarly journals Glycogen synthase kinase 3β inhibitors induce apoptosis in ovarian cancer cells and inhibit in-vivo tumor growth

2011 ◽  
pp. 1 ◽  
Author(s):  
Tyvette S. Hilliard ◽  
Irina N. Gaisina ◽  
Amanda G. Muehlbauer ◽  
Arsen M. Gaisin ◽  
Franck Gallier ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Ovarian Cancer Cells ◽  
Glycogen Synthase Kinase 3Β

scholarly journals SPR965, a Dual PI3K/mTOR Inhibitor, as a Targeted Therapy in Ovarian Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Arthur-Quan Tran ◽  
Stephanie A. Sullivan ◽  
Leo Li-Ying Chan ◽  
Yajie Yin ◽  
Wenchuan Sun ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Transition Process ◽  
Ovarian Cancer Cells ◽  
Serous Ovarian Cancer ◽  
Mesenchymal Transition

SPR965 is an inhibitor of PI3K and mTOR C1/C2 and has demonstrated anti-tumorigenic activity in a variety of solid tumors. We sought to determine the effects of SPR965 on cell proliferation and tumor growth in human serous ovarian cancer cell lines and a transgenic mouse model of high grade serous ovarian cancer (KpB model) and identify the underlying mechanisms by which SPR965 inhibits cell and tumor growth. SPR965 showed marked anti-proliferative activity by causing cell cycle arrest and inducing cellular stress in ovarian cancer cells. Treatment with SPR965 significantly inhibited tumor growth in KpB mice, accompanied by downregulation of Ki67 and VEGF and upregulation of Bip expression in ovarian tumors. SPR965 also inhibited adhesion and invasion through induction of the epithelial–mesenchymal transition process. As expected, downregulation of phosphorylation of AKT and S6 was observed in SPR965-treated ovarian cancer cells and tumors. Our results suggest that SPR965 has significant anti-tumorigenic effects in serous ovarian cancer in vitro and in vivo. Thus, SPR965 should be evaluated as a promising targeted agent in future clinical trials of ovarian cancer.

Novel organo-osmium(ii) proteosynthesis inhibitors active against human ovarian cancer cells reduce gonad tumor growth in Caenorhabditis elegans

2021 ◽  
Vol 8 (1) ◽  
pp. 141-155
Author(s):  
Enrique Ortega ◽  
Francisco J. Ballester ◽  
Alba Hernández-García ◽  
Samanta Hernández-García ◽  
M. Alejandra Guerrero-Rubio ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Antitumor Activity ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Arene Complexes ◽  
C Elegans

Novel Os(ii) arene complexes with a deprotonated ppy or ppy-CHO C^N ligand have been synthesized to selectively act on cancer cells as proteosynthesis inhibitors in vitro and exert antitumor activity in vivo in C. elegans models.

scholarly journals NSAIDs induce apoptosis in nonproliferating ovarian cancer cells and inhibit tumor growth in vivo

IUBMB Life ◽  
2012 ◽  
Vol 64 (7) ◽  
pp. 636-643 ◽  
Author(s):  
Kristal Duncan ◽  
Henriette Uwimpuhwe ◽  
Akos Czibere ◽  
Devanand Sarkar ◽  
Towia A. Libermann ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Inhibit Tumor Growth

scholarly journals Anti-Müllerian hormone (AMH) autocrine signaling promotes survival and proliferation of ovarian cancer cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maëva Chauvin ◽  
Véronique Garambois ◽  
Pierre-Emmanuel Colombo ◽  
Myriam Chentouf ◽  
Laurent Gros ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Growth ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Clonogenic Survival ◽  
Ovarian Cancer Cells ◽  
Physiological Range

AbstractIn ovarian carcinoma, anti-Müllerian hormone (AMH) type II receptor (AMHRII) and the AMH/AMHRII signaling pathway are potential therapeutic targets. Here, AMH dose-dependent effect on signaling and proliferation was analyzed in four ovarian cancer cell lines, including sex cord stromal/granulosa cell tumors and high grade serous adenocarcinomas (COV434-AMHRII, SKOV3-AMHRII, OVCAR8 and KGN). As previously shown, incubation with exogenous AMH at concentrations above the physiological range (12.5–25 nM) decreased cell viability. Conversely, physiological concentrations of endogenous AMH improved cancer cell viability. Partial AMH depletion by siRNAs was sufficient to reduce cell viability in all four cell lines, by 20% (OVCAR8 cells) to 40% (COV434-AMHRII cells). In the presence of AMH concentrations within the physiological range (5 to 15 pM), the newly developed anti-AMH B10 antibody decreased by 25% (OVCAR8) to 50% (KGN) cell viability at concentrations ranging between 3 and 333 nM. At 70 nM, B10 reduced clonogenic survival by 57.5%, 57.1%, 64.7% and 37.5% in COV434-AMHRII, SKOV3-AMHRII, OVCAR8 and KGN cells, respectively. In the four cell lines, B10 reduced AKT phosphorylation, and increased PARP and caspase 3 cleavage. These results were confirmed in ovarian cancer cells isolated from patients’ ascites, demonstrating the translational potential of these results. Furthermore, B10 reduced COV434-MISRII tumor growth in vivo and significantly enhanced the median survival time compared with vehicle (69 vs 60 days; p = 0.0173). Our data provide evidence for a novel pro-survival autocrine role of AMH in the context of ovarian cancer, which was targeted therapeutically using an anti-AMH antibody to successfully repress tumor growth.

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