Evidence map›Paper›PMID 22510946›Full record

ArticleInternational journal of cancer2012

The circadian clock gene BMAL1 is a novel therapeutic target for malignant pleural mesothelioma.

Momen Elshazley, Mitsuo Sato, Tetsunari Hase, Ryo Yamashita, Kenya Yoshida, Shinya Toyokuni, Futoshi Ishiguro, Hirotaka Osada, Yoshitaka Sekido, Kohei Yokoi and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-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

36 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. New Insights Into Cancer Chronotherapies.Frontiers in pharmacology · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. International journal of molecular sciences · 2020
    Article
  16. Article
  17. SR9009 has REV-ERB-independent effects on cell proliferation and metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Circadian (De)regulation in Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2019
    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

16 authors at 3 institutions in 2 countries.

Momen ElshazleyDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Aichi, Japan.
Mitsuo Sato
Tetsunari Hase
Ryo Yamashita
Kenya Yoshida
Shinya Toyokuni
Futoshi Ishiguro
Hirotaka Osada
Yoshitaka Sekido
Kohei Yokoi
Noriyasu Usami
David S Shames
Masashi Kondo
Adi F Gazdar
John D Minna
Yoshinori Hasegawa
Nagoya University · JPAichi Cancer Center · JPThe University of Texas Southwestern Medical Center · US

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
NCI NIH HHS P50 CA070907
6 · The paper itself

Abstract

Malignant pleural mesothelioma (MPM) is a highly aggressive neoplasm arising from the mesothelial cells lining the parietal pleura and it exhibits poor prognosis. Although there has been significant progress in MPM treatment, development of more efficient therapeutic approaches is needed. BMAL1 is a core component of the circadian clock machinery and its constitutive overexpression in MPM has been reported. Here, we demonstrate that BMAL1 may serve as a molecular target for MPM. The majority of MPM cell lines and a subset of MPM clinical specimens expressed higher levels of BMAL1 compared to a nontumorigenic mesothelial cell line (MeT-5A) and normal parietal pleural specimens, respectively. A serum shock induced a rhythmical BMAL1 expression change in MeT-5A but not in ACC-MESO-1, suggesting that the circadian rhythm pathway is deregulated in MPM cells. BMAL1 knockdown suppressed proliferation and anchorage-dependent and independent clonal growth in two MPM cell lines (ACC-MESO-1 and H290) but not in MeT-5A. Notably, BMAL1 depletion resulted in cell cycle disruption with a substantial increase in apoptotic and polyploidy cell population in association with downregulation of Wee1, cyclin B and p21(WAF1/CIP1) and upregulation of cyclin E expression. BMAL1 knockdown induced mitotic catastrophe as denoted by disruption of cell cycle regulators and induction of drastic morphological changes including micronucleation and multiple nuclei in ACC-MESO-1 cells that expressed the highest level of BMAL1. Taken together, these findings indicate that BMAL1 has a critical role in MPM and could serve as an attractive therapeutic target for MPM.

Indexed as

AgedApoptosisARNTL Transcription FactorsBlotting, WesternCell Line, TumorCell ProliferationCircadian RhythmFemaleFluorescent Antibody TechniqueGene Expression ProfilingGene Knockdown TechniquesHumansMaleMesotheliomaMiddle AgedPleural NeoplasmsARNTL Transcription FactorsBMAL1 protein, humanRNA, Small Interfering

Identifiers

PMID22510946
PMCPMC3479344
OpenAlexW2111110637

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.