ArticleProceedings of the National Academy of Sciences of the United States of America2008
Distinct nuclear and cytoplasmic functions of androgen receptor cofactor p44 and association with androgen-independent prostate cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 72 citations in OpenAlex.
- Disrupting the interaction between androgen receptor and its coregulator WDR77 delays the growth of treatment-resistant prostate cancer.Cell reports · 2025Article
- The Role of WDR77 in Cancer: More than a PRMT5 Interactor.Molecular cancer research : MCR · 2025Review
- WDR77 inhibits prion-like aggregation of MAVS to limit antiviral innate immune response.Nature communications · 2023Article
- A hotspot for posttranslational modifications on the androgen receptor dimer interface drives pathology and anti-androgen resistance.Science advances · 2023Article
- Article
- Germ-line mutations inProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Sulforaphane inhibits PRMT5 and MEP50 function to suppress the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2021Article
- WD Repeat Domain 77 Protein Regulates Translation of E2F1 and E2F3 mRNA.Molecular and cellular biology · 2020Article
- Protein arginine methyltransferase 5: A novel therapeutic target for triple-negative breast cancers.Cancer medicine · 2019Article
- The essential role of WD repeat domain 77 in prostate tumor initiation induced by Pten loss.Oncogene · 2018Article
- The PRMT5/WDR77 complex regulates alternative splicing through ZNF326 in breast cancer.Nucleic acids research · 2017Article
- Article
- Rationale for the development of alternative forms of androgen deprivation therapy.Endocrine-related cancer · 2017Review
- Sulforaphane suppresses PRMT5/MEP50 function in epidermal squamous cell carcinoma leading to reduced tumor formation.Carcinogenesis · 2017Article
- Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Protein arginine methyltransferase 5 regulates multiple signaling pathways to promote lung cancer cell proliferation.BMC cancer · 2016Article
- E2F and GATA switches turn off WD repeat domain 77 expression in differentiating cells.The Biochemical journal · 2016Article
- Cytoplasmic, full length and novel cleaved variant, TBLR1 reduces apoptosis in prostate cancer under androgen deprivation.Oncotarget · 2016Article
- GLI pathogenesis-related 1 functions as a tumor-suppressor in lung cancer.Molecular cancer · 2016Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Androgen receptor (AR) mediates transcriptional activation of diverse target genes through interactions with various coactivators that may alter its function and help mediate the switch between prostate cell proliferation and differentiation. We recently identified p44/MEP50 as an AR coactivator and further showed that it is expressed primarily in the nucleus and cytoplasm of benign prostate epithelial and prostate cancer cells, respectively. We also showed that haploinsufficiency in p44(+/-) mice causes prostate epithelial cell proliferation. To establish direct cause-and-effect relationships, we have used p44 fusion proteins that are selectively expressed in the nucleus or cytoplasm of prostate cancer cells (LNCaP), along with RNAi analyses, to examine effects of p44 both in vitro and in vivo (in tumor xenografts). We show that preferential expression of p44 in the nucleus inhibits proliferation of LNCaP cells in an AR-dependent manner, whereas preferential expression of p44 in the cytoplasm enhances cell proliferation. These effects appear to be mediated, at least in part, through the regulation of distinct cell-cycle regulatory genes that include p21 (up-regulated by nuclear p44) and cyclin D2 and CDK6 (up-regulated by cytoplasmic p44). Importantly, we also demonstrate that altered p44 expression is associated with androgen-independent prostate cancer. Our results indicate that nuclear p44 and cytoplasmic p44 have distinct and opposing functions in the regulation of prostate cancer cell proliferation.
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.