scholarly journals Synergistic inhibition of ovarian cancer cell growth by combining selective PI3K/mTOR and RAS/ERK pathway inhibitors

2013 ◽  
Vol 49 (18) ◽  
pp. 3936-3944 ◽  
Author(s):  
Karen E. Sheppard ◽  
Carleen Cullinane ◽  
Katherine M. Hannan ◽  
Meaghan Wall ◽  
Joanna Chan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Erk Pathway ◽  
Cancer Cell Growth ◽  
Synergistic Inhibition

scholarly journals Structural Bases for the Synergistic Inhibition of Human Thymidylate Synthase and Ovarian Cancer Cell Growth by Drug Combinations

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2061
Author(s):  
Cecilia Pozzi ◽  
Matteo Santucci ◽  
Gaetano Marverti ◽  
Domenico D’Arca ◽  
Lorenzo Tagliazucchi ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Thymidylate Synthase ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Preclinical Research ◽  
Cancer Cell Growth ◽  
X Ray ◽  
Synergistic Inhibition

Combining drugs represent an approach to efficiently prevent and overcome drug resistance and to reduce toxicity; yet it is a highly challenging task, particularly if combinations of inhibitors of the same enzyme target are considered. To show that crystallographic and inhibition kinetic information can provide indicators of cancer cell growth inhibition by combinations of two anti-human thymidylate synthase (hTS) drugs, we obtained the X-ray crystal structure of the hTS:raltitrexed:5-fluorodeoxyuridine monophosphate (FdUMP) complex. Its analysis showed a ternary complex with both molecules strongly bound inside the enzyme catalytic cavity. The synergistic inhibition of hTS and its mechanistic rationale were consistent with the structural analysis. When administered in combination to A2780 and A2780/CP ovarian cancer cells, the two drugs inhibited ovarian cancer cell growth additively/synergistically. Together, these results support the idea that X-ray crystallography can provide structural indicators for designing combinations of hTS (or any other target)-directed drugs to accelerate preclinical research for therapeutic application.

scholarly journals Drug-induced inactivation or gene silencing of class I histone deacetylases suppresses ovarian cancer cell growth: Implications for therapy

2007 ◽  
Vol 6 (5) ◽  
pp. 795-801 ◽  
Author(s):  
Dineo Khabele ◽  
Deok-Soo Son ◽  
Angelika K. Parl ◽  
Gary L. Goldberg ◽  
Leonard H. Augenlicht ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Gene Silencing ◽  
Cancer Cell ◽  
Histone Deacetylases ◽  
Ovarian Cancer Cell ◽  
Class I ◽  
Cancer Cell Growth ◽  
Drug Induced ◽  
Or Gene

scholarly journals FSH stimulates ovarian cancer cell growth by action on growth factor variant receptor

2007 ◽  
Vol 267 (1-2) ◽  
pp. 26-37 ◽  
Author(s):  
Y. Li ◽  
S. Ganta ◽  
C. Cheng ◽  
R. Craig ◽  
R.R. Ganta ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Growth

scholarly journals BRDT promotes ovarian cancer cell growth

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Ling Chen ◽  
Shang Cai ◽  
Jing-mei Wang ◽  
Ying-ying Huai ◽  
Pei-Hua Lu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Scid Mice ◽  
Ovarian Cancer Cells ◽  
Cancer Cell Growth ◽  
Primary Ovarian Cancer ◽  
And Migration ◽  
Proliferation And Migration

AbstractBromodomain testis-specific factor (BRDT) is a member of the bromodomain and extra-terminal (BET) family proteins. Its expression and potential functions in ovarian cancer were examined. We show that BRDT is overexpressed in human ovarian cancer tissues and in established (CaOV3)/primary ovarian cancer cells. However, its expression is low in ovarian epithelial tissues and cells. Significantly, shRNA-induced silencing or CRISPR/Cas9-mediated knockout of BRDT inhibited ovarian cancer cell growth, viability, proliferation and migration, and induced significant apoptosis activation. Conversely, exogenous overexpression of BRDT, by a lentiviral construct, augmented CaOV3 cell proliferation and migration. In CaOV3 cells expression of two key BRDT target genes, polo-like kinase 1 (PLK1) and aurora kinase C (AURKC), was downregulated by BRDT shRNA or knockout, but upregulated with BRDT overexpression. In vivo, xenograft tumors-derived from BRDT-knockout CaOV3 cells grew significantly slower than control tumors in severe combined immunodeficient (SCID) mice. Furthermore, intratumoral injection of BRDT shRNA lentivirus potently inhibited the growth of primary ovarian cancer xenografts in SCID mice. Downregulation of PLK1 and AURKC was detected in BRDT-knockout and BRDT-silenced tumor tissues. Collectively, BRDT overexpression promotes ovarian cancer cell progression. Targeting BRDT could be a novel strategy to treat ovarian cancer.

Abstract 4410: LSR promotes ovarian cancer cell growth following the activation of β-oxidation and its antibody inhibits lipid catabolism

2017 ◽  
Author(s):  
Kosuke Hiramatsu ◽  
Satoshi Serada ◽  
Takayuki Enomoto ◽  
Takuhei Yokoyama ◽  
Yusuke Takahashi ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Growth ◽  
Lipid Catabolism
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