Evidence map›Paper›PMID 20856200›Full record

ArticleOncogene2011

Vimentin is a novel AKT1 target mediating motility and invasion.

Q-S Zhu, K Rosenblatt, K-L Huang, G Lahat, R Brobey, S Bolshakov, T Nguyen, Z Ding, R Belousov, K Bill and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

137 citing papers in PubMed, 246 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Heliyon · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

77 more citing papers are in PubMed but not listed here.

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

16 authors at 6 institutions in 2 countries.

Q-S ZhuDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
K Rosenblatt
K-L Huang
G Lahat
R Brobey
S Bolshakov
T Nguyen
Z Ding
R Belousov
K Bill
X Luo
A Lazar
A Dicker
G B Mills
M-C Hung
D Lev
The University of Texas MD Anderson Cancer Center · USBrown Foundation · USChina Medical University · TWSidney Kimmel Cancer Center · USThe University of Texas at Austin · USThe University of Texas Medical Branch at Galveston · US

Funding

AKT-Vimentin interaction; a potential role in soft tissue sarcoma progression andR01CA138345 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BARELI, MENASHE · 2009 to 2013
$1.6M
NHLBI PROTEOMICS INITIATIVE-N01HV28184N01HV028184 · HV · UNIV OF TEXAS MEDICAL BRANCH · PI KUROSKY, ALEXANDER NONE · 2002 to 2006
–
NCI NIH HHS CA138345NCI NIH HHS R01 CA138345NHLBI NIH HHS N01 HV028184NHLBI NIH HHS N01-HV-28184
6 · The paper itself

Abstract

The PI3K/AKT signaling pathway is aberrant in a wide variety of cancers. Downstream effectors of AKT are involved in survival, growth and metabolic-related pathways. In contrast, contradictory data relating to AKT effects on cell motility and invasion, crucial prometastatic processes, have been reported pointing to a potential cell type and isoform type-specific AKT-driven function. By implication, study of AKT signaling should optimally be conducted in an appropriate intracellular environment. Prognosis in soft-tissue sarcoma (STS), the aggressive malignancies of mesenchymal origin, is poor, reflecting our modest ability to control metastasis, an effort hampered by lack of insight into molecular mechanisms driving STS progression and dissemination. We examined the impact of the cancer progression-relevant AKT pathway on the mesenchymal tumor cell internal milieu. We demonstrate that AKT1 activation induces STS cell motility and invasiveness at least partially through a novel interaction with the intermediate filament vimentin (Vim). The binding of AKT (tail region) to Vim (head region) results in Vim Ser39 phosphorylation enhancing the ability of Vim to induce motility and invasion while protecting Vim from caspase-induced proteolysis. Moreover, vimentin phosphorylation was shown to enhance tumor and metastasis growth in vivo. Insights into this mesenchymal-related molecular mechanism may facilitate the development of critically lacking therapeutic options for these devastating malignancies.

Indexed as

Cell MovementAnimalsBlotting, WesternCell Line, TumorFluorescent Antibody TechniqueHumansImmunoprecipitationMesodermMiceMice, SCIDNeoplasm InvasivenessProto-Oncogene Proteins c-aktSarcomaSignal TransductionSoft Tissue NeoplasmsTransfectionProto-Oncogene Proteins c-aktVimentin

Identifiers

PMID20856200
PMCPMC3010301
OpenAlexW2014331589

What OpenQuestion holds

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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.