ArticleThe Prostate2007
Prostate cancer cells tolerate a narrow range of androgen receptor expression and activity.
Article in The Prostate, 2007. 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, 30 citations in OpenAlex.
- Roles and therapeutic potential of the SLC family in prostate cancer-literature review.BMC urology · 2025Review
- Antiandrogenic Effects of a Polyphenol inInternational journal of molecular sciences · 2022Article
- Discovery proteomics defines androgen-regulated glycoprotein networks in prostate cancer cells, as well as putative biomarkers of prostatic diseases.Scientific reports · 2021Article
- Curcumin against Prostate Cancer: Current Evidence.Biomolecules · 2020Review
- Transient exposure to androgens induces a remarkable self-sustained quiescent state in dispersed prostate cancer cells.Cell cycle (Georgetown, Tex.) · 2017Article
- High expression of TROP2 characterizes different cell subpopulations in androgen-sensitive and androgen-independent prostate cancer cells.Oncotarget · 2016Article
- ARTIK-52 induces replication-dependent DNA damage and p53 activation exclusively in cells of prostate and breast cancer origin.Cell cycle (Georgetown, Tex.) · 2016Article
- Adenovirus-Mediated Angiotensin II Type 2 Receptor Overexpression Inhibits Tumor Growth of Prostate Cancer In Vivo.Journal of Cancer · 2016Article
- Article
- Negative regulation of the androgen receptor gene through a primate-specific androgen response element present in the 5' UTR.Hormones & cancer · 2014Article
- Characterization of tumor differentiation factor (TDF) and its receptor (TDF-R).Cellular and molecular life sciences : CMLS · 2013Review
- ARF represses androgen receptor transactivation in prostate cancer.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Targeting of Androgen Receptor Expression by Andro-miRs as Novel Adjunctive Therapeutics in Prostate Cancer.Journal of cancer therapy · 2013Article
- A regulatory feedback loop between Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and the androgen receptor in prostate cancer progression.The Journal of biological chemistry · 2012Article
- Article
- Recent progress in targeting cancer.Aging · 2011Review
- The androgen receptor induces integrin α6β1 to promote prostate tumor cell survival via NF-κB and Bcl-xL Independently of PI3K signaling.Cancer research · 2011Article
- Modulation of androgen receptor signaling in hormonal therapy-resistant prostate cancer cell lines.PloS one · 2011Article
- CDK9 regulates AR promoter selectivity and cell growth through serine 81 phosphorylation.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Bypass mechanisms of the androgen receptor pathway in therapy-resistant prostate cancer cell models.PloS one · 2010Article
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
Abstract
backgroundThe precise role of androgen receptor (AR) in the normal development of prostate and the progression of prostate cancer (CaP) remains controversial. While AR expression and activity is associated with growth arrest and differentiation of normal prostate cells, it is maintained in CaP cells that are characterized by continued proliferation. Our objective was to determine the importance of AR signaling for survival and growth of CaP cells, particularly those with a hormone-refractory phenotype.
methodAR expression was modulated in androgen-sensitive (AS) and androgen-insensitive (AI) CaP cells using RNAi and cDNA transduction. Resulting changes in AR transcriptional activity and cell growth were quantified.
resultsInterference with AR expression in both AS and AI CaP cells by shRNA transduction demonstrated a direct correlation between residual AR expression and cell viability. CaP cells lacking AR expression undergo apoptosis several days after AR down-regulation. This delayed response suggests that AR regulates apoptosis likely through an indirect mechanism. Overexpression of AR or hyper-stimulation of AR with high levels of androgen was also poorly tolerated by CaP cells. Cells with elevated AR had a growth disadvantage due to G1 cell cycle arrest and induction of p21 and GADD45 expression.
conclusionsCaP cells expressing endogenous AR are sensitive to both increases and decreases in AR expression levels and activity. AR in CaP cells is delicately regulated to provide a balance between cell death and continued proliferation. Thus, both approaches, inhibition and over-stimulation of AR activity, may have therapeutic value for treatment of prostate cancer.
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.