ArticleOncology letters2018
Anti-Müllerian hormone inhibits proliferation and induces apoptosis in epithelial ovarian cancer cells by regulating the cell cycle and decreasing the secretion of stem cell factor.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Anti-Müllerian hormone type II receptor protein expression in non-small cell lung cancer and the effect of AMH/AMHR2 signaling on cancer cell proliferation.Thoracic cancer · 2024Article
- Bone Morphogenetic Protein Signaling in Cancer; Some Topics in the Recent 10 Years.Frontiers in cell and developmental biology · 2022Review
- RNA expression differences in prostate tumors and tumor-adjacent stroma between Black and White Americans.Oncotarget · 2021Article
- AMH and Its Clinical Implications.Journal of obstetrics and gynaecology of India · 2020Review
- ACVR1 Function in Health and Disease.Cells · 2019Review
- Stage-specific modulation of antimüllerian hormone promotes primate follicular development and oocyte maturation in the matrix-free three-dimensional culture.Fertility and sterility · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-Müllerian hormone (AMH) has been demonstrated to exhibit an inhibitory effect on the proliferation, invasion, metastasis and drug resistance of ovarian cancer. However, the mechanisms underlying these effects remain unclear. In the present study, 10 µg/ml recombinant human AMH (rhAMH) was administered to human OVCAR3 and OVCAR8 epithelial ovarian cancer (EOC) cell lines. Cell proliferation, apoptosis and cell cycle were analyzed. The level of stem cell factor (SCF) was detected using a reverse transcription-quantitative polymerase chain reaction and an ELISA, respectively. The exogenous addition of rhAMH significantly reduced the proliferation of OVCAR3 and OVCAR8 cell lines compared with the control group (P<0.01). The apoptosis rate in the rhAMH treated group (48 h) significantly increased compared with in the control group (OVCAR3, P=0.035; OVCAR8, P=0.020). The apoptosis rate increased at 72 h but did not exhibit a significant difference when compared with the 48 h group (OVCAR3, P=0.145; OVCAR8, P=0.296). The percentage of cells in the G
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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.