Evidence map›Paper›PMID 22761335›Full record

ArticleCancer research2012

NAC1 is an actin-binding protein that is essential for effective cytokinesis in cancer cells.

Kai Lee Yap, Stephanie I Fraley, Michelle M Thiaville, Natini Jinawath, Kentaro Nakayama, Jianlong Wang, Tian-Li Wang, Denis Wirtz, Ie-Ming Shih

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Nacc1 Mutation in Mice Models Rare Neurodevelopmental Disorder with Underlying Synaptic Dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Review
  6. MiR-199a-3p promotes repair of myocardial infarction by targeting NACC2.International journal of clinical and experimental pathology · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Cancer Stem Cells or Tumor Survival Cells?Stem cells and development · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

9 authors at 3 institutions in 2 countries.

Kai Lee YapDepartment of Pathology, Pathobiology Graduate Program, Oncology Center, Johns Hopkins University, Baltimore, Maryland 21231, USA.
Stephanie I Fraley
Michelle M Thiaville
Natini Jinawath
Kentaro Nakayama
Jianlong Wang
Tian-Li Wang
Denis Wirtz
Ie-Ming Shih
Johns Hopkins University · USShimane University · JPMount Sinai Hospital · US

Funding

TRANS NETWORK PROJECTSU54CA143868 · NCI · JOHNS HOPKINS UNIVERSITY · PI SEARSON, PETER C · 2009 to 2013
$13.7M
Molecular Diagnostics for Malignant EffusionR01CA103937 · NCI · JOHNS HOPKINS UNIVERSITY · PI SHIH, IE-MING · 2004 to 2012
$2.7M
The Roles of HBXAP Gene in Ovarian CancerR01CA129080 · NCI · JOHNS HOPKINS UNIVERSITY · PI SHIH, IE-MING · 2008 to 2012
$1.7M
Characterizing Notch3 Signaling in Ovarian CancerR01CA148826 · NCI · JOHNS HOPKINS UNIVERSITY · PI WANG, TIAN-LI · 2011 to 2015
$1.7M
NCI NIH HHS R01 CA103937NCI NIH HHS R01CA103937NCI NIH HHS R01 CA129080NCI NIH HHS R01CA129080NCI NIH HHS R01 CA148826NCI NIH HHS R01CA148826NCI NIH HHS U54 CA143868NCI NIH HHS U54CA143868
6 · The paper itself

Abstract

NAC1 is a transcriptional corepressor protein that is essential to sustain cancer cell proliferation and migration. However, the underlying molecular mechanisms of NAC1 function in cancer cells remain unknown. In this study, we show that NAC1 functions as an actin monomer-binding protein. The conserved BTB protein interaction domain in NAC1 is the minimal region for actin binding. Disrupting NAC1 complex function by dominant-negative or siRNA strategies reduced cell retraction and abscission during late-stage cytokinesis, causing multinucleation in cancer cells. In Nac1-deficient murine fibroblasts, restoring NAC1 expression was sufficient to partially avert multinucleation. We found that siRNA-mediated silencing of the actin-binding protein profilin-1 in cancer cells caused a similar multinucleation phenotype and that NAC1 modulated the binding of actin to profillin-1. Taken together, our results indicate that the NAC1/actin/profilin-1 complex is crucial for cancer cell cytokinesis, with a variety of important biologic and clinical implications.

Indexed as

ActinsCytokinesisHEK293 CellsHeLa CellsHumansMCF-7 CellsNeoplasm ProteinsNeoplasmsPhenotypeProfilinsRepressor ProteinsActinsNACC1 protein, humanNeoplasm ProteinsPFN1 protein, humanProfilinsRepressor Proteins

Identifiers

PMID22761335
PMCPMC3421062
OpenAlexW2118581504

What OpenQuestion holds

Textmetadata
LicenceTDM
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.