Evidence map›Paper›PMID 27329840›Full record

ArticleOncotarget2016

Myosin 1e promotes breast cancer malignancy by enhancing tumor cell proliferation and stimulating tumor cell de-differentiation.

Jessica L Ouderkirk-Pecone, Gregory J Goreczny, Sharon E Chase, Arthur H Tatum, Christopher E Turner, Mira Krendel

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
2.1field-weighted citation impact, top 15% 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, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Study on the expression and prognostic relationship ofWorld journal of clinical oncology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Unconventional Myosins fromBiomolecules · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Long-Tailed Unconventional Class I Myosins in Health and Disease.International journal of molecular sciences · 2020
    Review
  18. Article
  19. Roles of Myosin-Mediated Membrane Trafficking in TGF-β Signaling.International journal of molecular sciences · 2019
    Review
  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

6 authors at 1 institution in 1 country.

Jessica L Ouderkirk-PeconeDepartment of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Gregory J GorecznyDepartment of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Sharon E ChaseDepartment of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Arthur H TatumDepartment of Pathology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Christopher E TurnerDepartment of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Mira KrendelDepartment of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
SUNY Upstate Medical University · US

Funding

Role of myosin 1e in podocyte biology and renal filtrationR01DK083345 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI Mira Krendel · 2011 to 2026
$6.8M
Paxillin and Hic-5 in Coordination of Cancer Cell Invasion MechanismsR01CA163296 · NCI · UPSTATE MEDICAL UNIVERSITY · PI TURNER, CHRISTOPHER E · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA163296NIDDK NIH HHS R01 DK083345
6 · The paper itself

Abstract

Despite advancing therapies, thousands of women die every year of breast cancer. Myosins, actin-dependent molecular motors, are likely to contribute to tumor formation and metastasis via their effects on cell adhesion and migration and may provide promising new targets for cancer therapies. Using the MMTV-PyMT murine model of breast cancer, we identified Myosin 1e (MYO1E) as a novel tumor promoter. Tumor latency in mice lacking MYO1E was significantly increased, and tumors formed in the absence of MYO1E displayed unusual papillary morphology, with well-differentiated layers of epithelial cells covering fibrovascular cores, rather than solid sheets of tumor cells typically observed in this cancer model. These tumors were reminiscent of papillary breast cancer in humans that is typically non-invasive and often cured by tumor excision. MYO1E-null tumors exhibited decreased expression of the markers of cell proliferation, which was recapitulated in primary tumor cells derived from MYO1E-null mice. In agreement with our findings, meta-analysis of patient survival data indicated that MYO1E expression level was associated with reduced recurrence-free survival in basal-like breast cancer. Overall, our data suggests that MYO1E contributes to breast tumor malignancy and regulates the differentiation and proliferation state of breast tumor cells.

Indexed as

AnimalsBreast NeoplasmsCell DedifferentiationCell ProliferationFemaleHumansKaplan-Meier EstimateMiceMice, Inbred C57BLMice, KnockoutMyosinsMyosin Type IPrognosisMyo1e protein, mouseMyosinsMyosin Type Ianimal models of cancerbreast cancermyosintherapeutic targetstumor promotion and progression

Identifiers

PMID27329840
PMCPMC5216807
OpenAlexW2441304977

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.