ArticleJournal of molecular histology2016
KDM3A confers metastasis and chemoresistance in epithelial ovarian cancer.
Article in Journal of molecular histology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 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
2 citing papers in PubMed, 5 citations in OpenAlex.
Corrections and comments
- Retraction · 2016-01-16Plagiarism of Data · · 2/13/2017
- Retracted
Authors and funding
0 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the association between KDM3A expression and the clinicopathological parameters of patients with epithelial ovarian cancer (EOC). KDM3A expression was analyzed using immunohistochemistry in EOC tissue microarray containing 90 paired cases of EOC and matched normal control. The expression level of KDM3A protein in EOC tissues was significantly higher than that of adjacent normal control tissues. In addition, positive expression of KDM3A correlated with the metastases. Furthermore, Kaplan-Meier survival analysis showed that a high expression level of KDM3A resulted in a significantly poor prognosis of EOC patients. Knock-down of KDM3A could suppress both the proliferation, migration and invasion in vitro EOC cell lines OV-2008 and ES-2. Additionally, knock-down of KDM3A not only could enhance cellular apoptosis induced by Cisplatin and Paclitaxel, but also induced some pro-apoptotic genes expression. Our data is the first to demonstrate that increased KDM3A expression in EOC is significantly associated with metastases and poor prognosis; and that KDM3A promotes the proliferation, migration and invasion of EOC cells. Knock-down of KDM3A may be an important complement to EOC that is resistant or refractory to chemotherapy.
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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.