Evidence map›Paper›PMID 22025562›Full record

ArticleCancer research2011

GLIPR1 suppresses prostate cancer development through targeted oncoprotein destruction.

Likun Li, Chengzhen Ren, Guang Yang, Elmoataz Abdel Fattah, Alexei A Goltsov, Soo Mi Kim, Ju-Seog Lee, Sanghee Park, Francesco J Demayo, Michael M Ittmann and 2 more

Abstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

28 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024
    Review
  3. Exploring the role of casein kinase 1α splice variants across cancer cell lines.Biochemical and biophysical research communications · 2024
    Article
  4. Review
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  9. Article
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  11. Review
  12. Article
  13. Article
  14. Review
  15. Casein Kinase 1α as a Regulator of Wnt-Driven Cancer.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Casein kinase 1α: biological mechanisms and theranostic potential.Cell communication and signaling : CCS · 2018
    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

12 authors at 3 institutions in 1 country.

Likun LiDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Chengzhen Ren
Guang Yang
Elmoataz Abdel Fattah
Alexei A Goltsov
Soo Mi Kim
Ju-Seog Lee
Sanghee Park
Francesco J Demayo
Michael M Ittmann
Patricia Troncoso
Timothy C Thompson
Michael E. DeBakey VA Medical Center · USThe University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Kathrin Milbury · 1985 to 2026
$290.8M
Targeting Tumor Microenvironment-Induced Therapy Resistance in Prostate Cancer Bone MetastasisP50CA140388 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGOTHETIS, CHRISTOPHER J. · 2009 to 2022
$23.4M
Progression/Oncogene Induced Prostate CancerR01CA050588 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMPSON, TIMOTHY CHARLES · 1989 to 2011
$3.5M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA140388NCI NIH HHS R01 CA050588PHS HHS P50140388PHS HHS R0150588
6 · The paper itself

Abstract

Downregulation of the proapoptotic p53 target gene glioma pathogenesis-related protein 1 (GLIPR1) occurs frequently in prostate cancer, but the functional meaning of this event is obscure. Here, we report the discovery of functional relationship between GLIPR1 and c-Myc in prostate cancer where c-Myc is often upregulated. We found that the expression of GLIPR1 and c-Myc were inversely correlated in human prostate cancer. Restoration of GLIPR1 expression in prostate cancer cells downregulated c-myc levels, inhibiting cell-cycle progression. Downregulation was linked to a reduction in β-catenin/TCF4-mediated transcription of the c-myc gene, which was caused by GLIPR1-mediated redistribution of casein kinase 1α (CK1α) from the Golgi apparatus to the cytoplasm where CK1α could phosphorylate β-catenin and mediate its destruction. In parallel, GLIPR1 also promoted c-Myc protein ubiquitination and degradation by glycogen synthase kinase-3α- and/or CK1α-mediated c-Myc phosphorylation. Notably, genetic ablation of the mouse homolog of Glipr1 cooperated with c-myc overexpression to induce prostatic intraepithelial neoplasia and prostate cancer. Together, our findings provide evidence for CK1α-mediated destruction of c-Myc and identify c-Myc S252 as a crucial CK1α phosphorylation site for c-Myc degradation. Furthermore, they reveal parallel mechanisms of c-myc downregulation by GLIPR1 that when ablated in the prostate are sufficient to drive c-Myc expression and malignant development.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBlotting, WesternCasein Kinase IalphaCell CycleCell Line, TumorDown-RegulationFemaleGene Expression ProfilingHumansImmunohistochemistryMaleMembrane ProteinsMiceMice, TransgenicCasein Kinase IalphaGLIPR1 protein, humanMembrane ProteinsNeoplasm ProteinsNerve Tissue ProteinsProto-Oncogene Proteins c-myc

Identifiers

PMID22025562
PMCPMC3813470
OpenAlexW2110560370

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.