ArticleInvestigational new drugs2012
Growth inhibition induced by antiprogestins RU-38486, ORG-31710, and CDB-2914 in ovarian cancer cells involves inhibition of cyclin dependent kinase 2.
Article in Investigational new drugs, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- The metastatic capacity of high-grade serous ovarian cancer cells changes along disease progression: inhibition by mifepristone.Cancer cell international · 2022Article
- CCM signaling complex (CSC) couples both classic and non-classic Progesterone receptor signaling.Cell communication and signaling : CCS · 2022Article
- CmPn signaling networks in the tumorigenesis of breast cancer.Frontiers in endocrinology · 2022Article
- CmP signaling network unveils novel biomarkers for triple negative breast cancer in African American women.Cancer biomarkers : section A of Disease markers · 2022Article
- Ulipristal acetate simultaneously provokes antiproliferative and proinflammatory responses in endometrial cancer cells.Heliyon · 2022Article
- Anticancer effects of mifepristone on human uveal melanoma cells.Cancer cell international · 2021Article
- The gold complex auranofin: new perspectives for cancer therapy.Discover oncology · 2021Review
- Giants and monsters: Unexpected characters in the story of cancer recurrence.Advances in cancer research · 2020Review
- Reproductive epidemiology of glial tumors may reveal novel treatments: high-dose progestins or progesterone antagonists as endocrino-immune modifiers against glioma.Neurosurgical review · 2019Review
- Advanced assessment of migration and invasion of cancer cells in response to mifepristone therapy using double fluorescence cytochemical labeling.BMC cancer · 2019Article
- Mifepristone inhibits non-small cell lung carcinoma cellular escape from DNA damaging cisplatin.Cancer cell international · 2018Article
- Mifepristone increases mRNA translation rate, triggers the unfolded protein response, increases autophagic flux, and kills ovarian cancer cells in combination with proteasome or lysosome inhibitors.Molecular oncology · 2016Article
- Antihormonal agents as a strategy to improve the effect of chemo-radiation in cervical cancer: in vitro and in vivo study.BMC cancer · 2015Article
- Antiprogestins in gynecological diseases.Reproduction (Cambridge, England) · 2015Review
- Resistance to cisplatin and paclitaxel does not affect the sensitivity of human ovarian cancer cells to antiprogestin-induced cytotoxicity.Journal of ovarian research · 2014Article
- Mifepristone improves chemo-radiation response in glioblastoma xenografts.Cancer cell international · 2013Article
- Article
- Synergistic lethality of mifepristone and LY294002 in ovarian cancer cells.Cancer growth and metastasis · 2013Article
- Drug Repurposing for Cancer Therapy.Journal of cancer science & therapy · 2012Article
- Mifepristone prevents repopulation of ovarian cancer cells escaping cisplatin-paclitaxel therapy.BMC cancer · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Antiprogestins have been largely utilized in reproductive medicine, yet their repositioning for oncologic use is rapidly emerging. In this study we investigated the molecular mediators of the anti-ovarian cancer activity of the structurally related antiprogestins RU-38486, ORG-31710 and CDB-2914. We studied the responses of wt p53 OV2008 and p53 null SK-OV-3 cells to varying doses of RU-38486, ORG-31710 and CDB-2914. The steroids inhibited the growth of both cell lines with a potency of RU-38486 > ORG-31710 > CDB-2914, and were cytostatic at lower doses but lethal at higher concentrations. Antiprogestin-induced lethality associated with morphological features of apoptosis, hypodiploid DNA content, DNA fragmentation, and cleavage of executer caspase substrate PARP. Cell death ensued despite RU-38486 caused transient up-regulation of anti-apoptotic Bcl-2, ORG-31710 induced transient up-regulation of inhibitor of apoptosis XIAP, and CDB-2914 up-regulated both XIAP and Bcl-2. The antiprogestins induced accumulation of Cdk inhibitors p21(cip1) and p27(kip1) and increased association of p21(cip1) and p27(kip1) with Cdk-2. They also promoted nuclear localization of p21(cip1) and p27(kip1), reduced the nuclear abundances of Cdk-2 and cyclin E, and blocked the activity of Cdk-2 in both nucleus and cytoplasm. The cytotoxic potency of the antiprogestins correlated with the magnitude of the inhibition of Cdk-2 activity, ranging from G1 cell cycle arrest towards cell death. Our results suggest that, as a consequence of their cytostatic and lethal effects, antiprogestin steroids of well-known contraceptive properties emerge as attractive new agents to be repositioned for ovarian cancer therapeutics.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.