Evidence map›Paper›PMID 31288154›Full record

ArticleiScience2019

mEAK-7 Forms an Alternative mTOR Complex with DNA-PKcs in Human Cancer.

Joe Truong Nguyen, Fatima Sarah Haidar, Alexandra Lucienne Fox, Connor Ray, Daniela Baccelli Mendonça, Jin Koo Kim, Paul H Krebsbach

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

25 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Anticancer Effect ofMolecules (Basel, Switzerland) · 2024
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. mTOR Signaling Components in Tumor Mechanobiology.International journal of molecular sciences · 2022
    Review
  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

7 authors at 2 institutions in 1 country.

Joe Truong NguyenDepartment of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48105, USA.
Fatima Sarah HaidarDepartment of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48105, USA.
Alexandra Lucienne FoxDepartment of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48105, USA.
Connor RayDepartment of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48105, USA.
Daniela Baccelli MendonçaDepartment of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109, USA.
Jin Koo KimSection of Periodontics, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Paul H KrebsbachSection of Periodontics, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: pkrebsbach@dentistry.ucla.edu.
University of Michigan · USUniversity of California, Los Angeles · US

Funding

Tissue Engineering and RegenerationT32DE007057 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID H. KOHN · 1985 to 2026
$17.3M
Osteoblast Lineage Progression from Embryonic Stem CellsR01DE016530 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAARTINEN, VESA M · 2005 to 2016
$3.9M
DNA damage activates non-canonical mTORC1 signaling through mammalian EAK-7 in HNSCC.F30DE026048 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NGUYEN, JOE TRUONG · 2016 to 2018
$145k
NIDCR NIH HHS F30 DE026048NIDCR NIH HHS R01 DE016530NIDCR NIH HHS T32 DE007057
6 · The paper itself

Abstract

MTOR associated protein, eak-7 homolog (mEAK-7), activates mechanistic target of rapamycin (mTOR) signaling in human cells through an alternative mTOR complex to regulate S6K2 and 4E-BP1. However, the role of mEAK-7 in human cancer has not yet been identified. We demonstrate that mEAK-7 and mTOR signaling are strongly elevated in tumor and metastatic lymph nodes of patients with non-small-cell lung carcinoma compared with those of patients with normal lung or lymph tissue. Cancer stem cells, CD44+/CD90+ cells, yield elevated mEAK-7 and activated mTOR signaling. mEAK-7 is required for clonogenic potential and spheroid formation. mEAK-7 associates with DNA-dependent protein kinase catalytic subunit isoform 1 (DNA-PKcs), and this interaction is increased in response to X-ray irradiation to regulate S6K2 signaling. DNA-PKcs pharmacologic inhibition or genetic knockout reduced S6K2, mEAK-7, and mTOR binding with DNA-PKcs, resulting in loss of S6K2 activity and mTOR signaling. Therefore, mEAK-7 forms an alternative mTOR complex with DNA-PKcs to regulate S6K2 in human cancer cells.

Indexed as

Biological SciencesCancerCell Biology

Identifiers

PMID31288154
PMCPMC6614755
OpenAlexW2954596349

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.