ArticleThe Journal of biological chemistry2012
Rad9 protein contributes to prostate tumor progression by promoting cell migration and anoikis resistance.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 38 citations in OpenAlex.
- BUB1-based risk model predicts prostate cancer prognosis and reveals therapeutic vulnerabilities.European journal of medical research · 2025Article
- AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024Review
- An anoikis-related gene signature for prediction of the prognosis in prostate cancer.Frontiers in oncology · 2023Article
- Anoikis in phenotypic reprogramming of the prostate tumor microenvironment.Frontiers in endocrinology · 2023Review
- Effect of AKT silence on malignant biological behavior of renal cell carcinoma cells.BMC urology · 2022Article
- HUS1 as a Potential Therapeutic Target in Urothelial Cancer.Journal of clinical medicine · 2022Article
- Hypermethylation ofEXCLI journal · 2022Article
- Short-chain L-3-hydroxyacyl-CoA dehydrogenase: A novel vital oncogene or tumor suppressor gene in cancers.Frontiers in pharmacology · 2022Review
- FOXP1 and NDRG1 act differentially as downstream effectors of RAD9-mediated prostate cancer cell functions.Cellular signalling · 2021Article
- DNMT1 and DNMT3B regulate tumorigenicity of human prostate cancer cells by controlling RAD9 expression through targeted methylation.Carcinogenesis · 2021Article
- RAD9A promotes metastatic phenotypes through transcriptional regulation of anterior gradient 2 (AGR2).Carcinogenesis · 2019Article
- Prostate cancer: unmet clinical needs and RAD9 as a candidate biomarker for patient management.Translational cancer research · 2018Article
- Rad9a is required for spermatogonia differentiation in mice.Oncotarget · 2016Article
- Article
- Regulation of NEIL1 protein abundance by RAD9 is important for efficient base excision repair.Nucleic acids research · 2015Article
- RAD9 enhances radioresistance of human prostate cancer cells through regulation of ITGB1 protein levels.The Prostate · 2014Article
- DNA damage response genes and the development of cancer metastasis.Radiation research · 2014Review
- Identification of RECQ1-regulated transcriptome uncovers a role of RECQ1 in regulation of cancer cell migration and invasion.Cell cycle (Georgetown, Tex.) · 2014Article
- CXCR7 is highly expressed in acute lymphoblastic leukemia and potentiates CXCR4 response to CXCL12.PloS one · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Rad9 as part of the Rad9-Hus1-Rad1 complex is known to participate in cell cycle checkpoint activation and DNA repair. However, Rad9 can act as a sequence-specific transcription factor, modulating expression of a number of genes. Importantly, Rad9 is up-regulated in prostate cancer cell lines and clinical specimens. Its expression correlates positively with advanced stage tumors and its down-regulation reduces tumor burden in mice. We show here that transient down-regulation of Rad9 by RNA interference reduces DU145 and PC3 prostate cancer cell proliferation and survival in vitro. In addition, transient or stable down-regulation of Rad9 impairs migration and invasion of the cells. Moreover, stable reduction of Rad9 renders DU145 cell growth anchorage-dependent. It also decreases expression of integrin β1 protein and sensitizes DU145 and LNCaP cells to anoikis and impairs Akt activation. On the other hand, stable expression of Mrad9, the mouse homolog, in DU145/shRNA Rad9 cells restores migration, invasion, anchorage-independent growth, integrin β1 expression, and anoikis resistance with a concomitant elevation of Akt activation. We thus demonstrate for the first time that Rad9 contributes to prostate tumorigenesis by increasing not only tumor proliferation and survival but also tumor migration and invasion, anoikis resistance, and anchorage-independent growth.
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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.