Evidence map›Paper›PMID 22473899›Full record

ArticleThe Prostate2012

MUC1-C oncoprotein confers androgen-independent growth of human prostate cancer cells.

Hasan Rajabi, Rehan Ahmad, Caining Jin, Maya Datt Joshi, Minakshi Guha, Maroof Alam, Surender Kharbanda, Donald Kufe

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Dependence on MUC1-C in Progression of Neuroendocrine Prostate Cancer.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. MUC1 in hematological malignancies.Leukemia & lymphoma · 2016
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Hasan RajabiDana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.
Rehan Ahmad
Caining Jin
Maya Datt Joshi
Minakshi Guha
Maroof Alam
Surender Kharbanda
Donald Kufe
Harvard University · USDana-Farber Cancer Institute · USGenus Oncology (United States) · US

Funding

Targeting the MUC1-C Oncoprotein in Triple-Negative Breast CancerR01CA097098 · NCI · DANA-FARBER CANCER INSTITUTE · PI DONALD W. KUFE · 2002 to 2026
$8.8M
MUC1-C Oncoprotein Evades Immune Destruction in Non-small Cell Lung CancerR01CA166480 · NCI · DANA-FARBER CANCER INST · PI KUFE, DONALD W., WONG, KWOK KIN · 2012 to 2021
$6.3M
DIFFERENTIATING AGENTS IN HEMATOLOGIC MALIGNANCIESR01CA042802 · NCI · DANA-FARBER CANCER INSTITUTE · PI KUFE, DONALD W. · 1986 to 2012
$3.8M
NCI NIH HHS CA42802NCI NIH HHS CA97098NCI NIH HHS R01 CA042802NCI NIH HHS R01 CA097098NCI NIH HHS R01 CA166480
6 · The paper itself

Abstract

backgroundThe mucin 1 (MUC1) heterodimeric oncoprotein is overexpressed in human prostate cancers with aggressive pathologic and clinical features. However, few insights are available regarding the functional role of MUC1 in prostate cancer.

methodsEffects of MUC1-C on androgen receptor (AR) expression were determined by RT-PCR, immunoblotting and AR promoter activation. Coimmunoprecipitations, direct binding assays, and chromatin immunoprecipitation (ChIP) studies were performed to assess the interaction between MUC1-C and AR. Cells were analyzed for invasion, growth in androgen-depleted medium, and sensitivity to MUC1-C inhibitors.

resultsThe present studies in androgen-dependent LNCaP and LAPC4 prostate cancer cells demonstrate that the oncogenic MUC1-C subunit suppresses AR expression. The results show that MUC1-C activates a posttranscriptional mechanism involving miR-135b-mediated downregulation of AR mRNA levels. The results further demonstrate that MUC1-C forms a complex with AR through a direct interaction between the MUC1-C cytoplasmic domain and the AR DNA-binding domain (DBD). In addition, MUC1-C associates with AR in a complex that occupies the PSA promoter. The interaction between MUC1-C and AR is associated with induction of the epithelial-mesenchymal transition (EMT) and increased invasion. MUC1-C also conferred growth in androgen-depleted medium and resistance to bicalutamide treatment. Moreover, expression of MUC1-C resulted in sensitivity to the MUC1-C inhibitor GO-203 with inhibition of growth in vitro. GO-203 treatment also inhibited growth of established tumor xenografts in nude mice.

conclusionsThese findings indicate that MUC1-C suppresses AR expression in prostate cancer cells and confers a more aggressive androgen-independent phenotype that is sensitive to MUC1-C inhibition.

Indexed as

AdenocarcinomaAndrogensCell ProliferationDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMaleMicroRNAsMolecular Targeted TherapyMucin-1Neoplasm InvasivenessProstatic NeoplasmsProtein BindingProtein Processing, Post-TranslationalReceptors, AndrogenAndrogensMicroRNAsMIRN135 microRNA, humanMUC1 protein, humanMucin-1Receptors, AndrogenRNA, Messenger

Identifiers

PMID22473899
PMCPMC3413781
OpenAlexW2117712992

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.