ArticleMolecular and cellular biology2004
Human checkpoint protein hRad9 functions as a negative coregulator to repress androgen receptor transactivation in prostate cancer cells.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 56 citations in OpenAlex.
- Construction and Validation of a Prognostic Model Based on Pyroptosis-related Genes in Bladder Cancer.Combinatorial chemistry & high throughput screening · 2024Article
- The Androgen Receptor Does Not Directly Regulate the Transcription of DNA Damage Response Genes.Molecular cancer research : MCR · 2023Article
- Article
- Prostate cancer: unmet clinical needs and RAD9 as a candidate biomarker for patient management.Translational cancer research · 2018Article
- ARTIK-52 induces replication-dependent DNA damage and p53 activation exclusively in cells of prostate and breast cancer origin.Cell cycle (Georgetown, Tex.) · 2016Article
- The convergence of DNA damage checkpoint pathways and androgen receptor signaling in prostate cancer.Endocrine-related cancer · 2014Review
- DNA damage response genes and the development of cancer metastasis.Radiation research · 2014Review
- Mechanism of androgen receptor corepression by CKβBP2/CRIF1, a multifunctional transcription factor coregulator expressed in prostate cancer.Molecular and cellular endocrinology · 2014Article
- Regulation of Androgen Receptor by E3 Ubiquitin Ligases: for More or Less.Receptors & clinical investigation · 2014Article
- ARF represses androgen receptor transactivation in prostate cancer.Molecular endocrinology (Baltimore, Md.) · 2013Article
- The role of RAD9 in tumorigenesis.Journal of molecular cell biology · 2011Review
- Analysis of interdomain interactions of the androgen receptor.Methods in molecular biology (Clifton, N.J.) · 2011Article
- Article
- Functional screening of FxxLF-like peptide motifs identifies SMARCD1/BAF60a as an androgen receptor cofactor that modulates TMPRSS2 expression.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Targeted deletion of Rad9 in mouse skin keratinocytes enhances genotoxin-induced tumor development.Cancer research · 2008Article
- Localization of hRad9 in breast cancer.BMC cancer · 2008Article
- Src kinase potentiates androgen receptor transactivation function and invasion of androgen-independent prostate cancer C4-2 cells.Oncogene · 2008Article
- Rad9 has a functional role in human prostate carcinogenesis.Cancer research · 2008Article
- Prohibitin, a protein downregulated by androgens, represses androgen receptor activity.Oncogene · 2007Article
- Receptor-interacting protein 140 is a repressor of the androgen receptor activity.Molecular endocrinology (Baltimore, Md.) · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Positive responses to combined androgen elimination therapy and radiation therapy have been well documented in the treatment of prostate cancer patients. The detailed mechanisms how androgen-androgen receptor (AR) cross talks to the radiation-related signal pathways, however, remain largely unknown. Here we report the identification of hRad9, a key member of the checkpoint Rad protein family, as a coregulator to suppress androgen-AR transactivation in prostate cancer cells. In vivo and in vitro interaction assays using Saccharomyces cerevisiae two-hybrid, mammalian two-hybrid, glutathione S-transferase pull-down, and coimmunoprecipitation methods prove that AR can interact with the C terminus of hRad9 via its ligand binding domain. The FXXLF motif within the C terminus of hRad9 interrupts the androgen-induced interaction between the N terminus and C terminus of AR. This interaction between AR and hRad9 may result in the suppression of AR transactivation, demonstrated by the repressed AR transactivation in androgen-induced luciferase reporter assay and the reduced endogenous prostate-specific antigen expression in Western blot assay. Addition of small interfering RNA of hRad9 can reverse hRad9 suppression effects, which suggests that hRad9 functions as a repressor of AR transactivation in vivo. Together, our data provide the first linkage between androgen-AR signals and radiation-induced responses. Further studies of the influence of hRad9 on prostate cancer growth may provide potential new therapeutic approaches.
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.