Evidence map›Paper›PMID 20086099›Full record

ArticleMolecular and cellular biology2010

14-3-3Tau regulates ubiquitin-independent proteasomal degradation of p21, a novel mechanism of p21 downregulation in breast cancer.

Bing Wang, Kang Liu, Hui-Yi Lin, Naresh Bellam, Shiyun Ling, Weei-Chin Lin

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 60 citations in OpenAlex.

  1. p57International journal of molecular sciences · 2024
    Article
  2. Article
  3. Article
  4. Review
  5. The crosstalk between ubiquitination and endocrine therapy.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
  6. 14-3-3τ drives estrogen receptor loss via ERα36 induction and GATA3 inhibition in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. [miR-16-5p regulates apoptosis and migration of drug-resistant breast cancer cells by targeting YWHAQ].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  8. Article
  9. The mechanobiome: a goldmine for cancer therapeutics.American journal of physiology. Cell physiology · 2021
    Review
  10. E2F1 sumoylation as a protective cellular mechanism in oxidative stress response.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Interaction between Rho GTPases and 14-3-3 Proteins.International journal of molecular sciences · 2017
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Bing WangDivision of Hematology and Oncology, Department of Medicine,1 Medical Statistics Section, University of Alabama at Birmingham, Birmingham, Alabama 35294-2182, USA.
Kang Liu
Hui-Yi Lin
Naresh Bellam
Shiyun Ling
Weei-Chin Lin
University of Alabama at Birmingham · US

Funding

The ATM/E2F1 Pathway in DNA Damage and Growth ControlR01CA100857 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIN, WEEI-CHIN · 2004 to 2019
$4.8M
Therapeutic Targeting of Oncogenic Stress in Cancer TreatmentR01CA138641 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LIN, WEEI-CHIN · 2010 to 2014
$1.5M
NCI NIH HHS CA 100857NCI NIH HHS R01 CA100857NCI NIH HHS R01 CA138641
6 · The paper itself

Abstract

14-3-3 proteins regulate many cellular functions, including proliferation. However, the detailed mechanisms by which they control the cell cycle remain to be fully elucidated. We report that one of the 14-3-3 isoforms, 14-3-3tau, is required for the G(1)/S transition through its role in ubiquitin-independent proteasomal degradation of p21. 14-3-3tau binds to p21, MDM2, and the C8 subunit of the 20S proteasome in G(1) phase and facilitates proteasomal targeting of p21. This function of 14-3-3tau may be deregulated in cancer. The overexpression of 14-3-3tau is frequently found in primary human breast cancer and correlates with lower levels of p21 and shorter patient survival. Tenascin-C, an extracellular matrix protein involved in tumor initiation and progression and a known 14-3-3tau inducer, decreases p21 and abrogates adriamycin-induced G(1)/S arrest. It has been known that p21 is required for a proper tamoxifen response in breast cancer. We show that the overexpression of 14-3-3tau inhibits tamoxifen-induced p21 induction and growth arrest in MCF7 cells. Together, the findings of our studies strongly suggest a novel oncogenic role of 14-3-3tau by downregulating p21 in breast cancer. Therefore, 14-3-3tau may be a potential therapeutic target in breast cancer.

Indexed as

Down-RegulationProtein Processing, Post-Translational14-3-3 ProteinsAnimalsBreast NeoplasmsCell LineCyclin-Dependent Kinase Inhibitor p21FemaleG1 PhaseHumansMiceProteasome Endopeptidase ComplexProtein BindingProtein StabilityProtein SubunitsProto-Oncogene Proteins c-mdm214-3-3 ProteinsCyclin-Dependent Kinase Inhibitor p21MDM2 protein, humanProteasome Endopeptidase ComplexProtein SubunitsProto-Oncogene Proteins c-mdm2TamoxifenTenascinUbiquitin

Identifiers

PMID20086099
PMCPMC2832502
OpenAlexW2101040637

What Socratic holds

Textmetadata
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 Socratic graph.