Evidence map›Paper›PMID 25373736›Full record

ArticleOncotarget2014

Mastl kinase, a promising therapeutic target, promotes cancer recurrence.

Ling Wang, Vivian Q Luong, Peter J Giannini, Aimin Peng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

35 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. The ATM-E6AP-MASTL axis mediates DNA damage checkpoint recovery.bioRxiv : the preprint server for biology · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  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

4 authors at 1 institution in 1 country.

Ling WangDepartment of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln, NE 68583.
Vivian Q LuongDepartment of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln, NE 68583.
Peter J GianniniDepartment of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln, NE 68583.
Aimin PengDepartment of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln, NE 68583.
University of Nebraska Medical Center · US

Funding

Nebraska Center for Cellular SignalingP20GM103489 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2012 to 2012
$2.0M
DNA Damage Checkpoint Recovery and CancerR01CA172574 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PENG, AIMIN · 2013 to 2017
$1.6M
NCI NIH HHS 1R01CA172574NCI NIH HHS R01 CA172574NIGMS NIH HHS 5P20GM103489NIGMS NIH HHS P20 GM103489
6 · The paper itself

Abstract

Mastl kinase promotes mitotic progression and cell cycle reentry after DNA damage. We report here that Mastl is frequently upregulated in various types of cancer. This upregulation was correlated with cancer progression in breast and oral cancer, poor patient survival in breast cancer, and tumor recurrence in head and neck squamous cell carcinoma. We further investigated the role of Mastl in tumor resistance using cell lines derived from the initial and recurrent tumors of the same head and neck squamous cell carcinoma patients. Ectopic expression of Mastl in the initial tumor cells strongly promoted cell proliferation in the presence of cisplatin by attenuating DNA damage signaling and cell death. Mastl knockdown in recurrent tumor cells re-sensitized their response to cancer therapy in vitro and in vivo. Finally, Mastl targeting specifically potentiated cancer cells to cell death in chemotherapy while sparing normal cells. Thus, this study revealed that Mastl upregulation is involved in cancer progression and tumor recurrence after initial cancer therapy, and validated Mastl as a promising target to increase the therapeutic window.

Indexed as

Gene Expression Regulation, NeoplasticAgedAnimalsCarcinoma, Squamous CellCell Line, TumorCell ProliferationCisplatinDisease ProgressionDNA DamageEpitopesFemaleHumansImmunohistochemistryMaleMiceMice, NudeCisplatinEpitopesMASTL protein, humanMicrotubule-Associated ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID25373736
PMCPMC4294390
OpenAlexW2159137685

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.