ArticleJournal of cancer research and clinical oncology2012
N-myc downstream-regulated gene 1/Cap43 may function as tumor suppressor in endometrial cancer.
Article in Journal of cancer research and clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Targeting c-MYC: a potential non-hormonal therapeutic approach for endometriosis treatment.Frontiers in cell and developmental biology · 2023Article
- Article
- Iron-Chelation Treatment by Novel Thiosemicarbazone Targets Major Signaling Pathways in Neuroblastoma.International journal of molecular sciences · 2021Article
- Molecular Interplays Between Cell Invasion and Radioresistance That Lead to Poor Prognosis in Head-Neck Cancer.Frontiers in oncology · 2021Article
- NDRG1 Controls Gastric Cancer Migration and Invasion through Regulating MMP-9.Pathology oncology research : POR · 2016Article
- The molecular effect of metastasis suppressors on Src signaling and tumorigenesis: new therapeutic targets.Oncotarget · 2015Review
- Evaluation of a hypoxia regulated gene panel in ovarian cancer.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2015Article
- Novel therapeutic targets for pancreatic cancer.World journal of gastroenterology · 2014Review
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeN-myc downstream-regulated gene 1 (NDRG1) reportedly regulates tumor progression in various cancers. Our previous studies showed that NDRG1 was aberrantly overexpressed in human endometrial cancer tissues. The purpose of the present study was to investigate the role of NDRG1 in endometrial carcinogenesis.
methodsA short hairpin RNA (shRNA)-mediated gene silencing strategy was employed to stably suppress the expression of NDRG1 in endometrial cancer Ishikawa cells. The influence of NDRG1 silencing on cancer cell biological behaviors was examined through observing in vitro tumor cell proliferation, colony formation, cell migration and invasion. Moreover, the mammalian NDRG1 expression vector pcDNA3.1(+)/NDRG1 was constructed to determine the effects of NDRG1 overexpression on cell proliferation and migration. Additionally, gene expression microarray analysis was conducted to identify NDRG1 downstream target genes after NDRG1 knockdown.
resultsIt was demonstrated that NDRG1 knockdown significantly enhanced Ishikawa cell proliferation and dramatically promoted cell migration and invasion. Furthermore, overexpression of NDRG1 in Ishikawa cells greatly inhibited cell proliferation and migration. Through microarray analysis and data mining, a large cohort of NDRG1-repressed target genes were identified. Additionally, through comparing the current microarray results with those obtained previously in studies of cervical and ovarian cancer cells conducted by us, 19 more specific common downstream target genes were identified.
conclusionsIt was demonstrated that NDRG1 might carry out a tumor suppressor function during endometrial carcinogenesis. The identification of downstream target genes should afford meaningful hints for prospective investigations. The tumor suppressor function of NDRG1 may open a new window for the target therapy of endometrial cancer.
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