Evidence map›Paper›PMID 28925397›Full record

ArticleOncogene2018

Coactosin-like protein CLP/Cotl1 suppresses breast cancer growth through activation of IL-24/PERP and inhibition of non-canonical TGFβ signaling.

L Xia, X Xiao, W L Liu, Y Song, T J J Liu, Y J Li, E Zacksenhaus, X J Hao, Y Ben-David

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Sex differences in human pre-gastrulation embryos.Science China. Life sciences · 2025
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  7. Spatially ResolvedbioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Coactosin-Like Protein in Breast Carcinoma: Friend or Foe?Journal of inflammation research · 2022
    Article
  18. Article
  19. Long noncoding RNAMolecular therapy. Nucleic acids · 2021
    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 4 institutions in 2 countries.

L XiaState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, PR China.
X XiaoState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, PR China.
W L LiuState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, PR China.
Y SongState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, PR China.
T J J LiuState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, PR China.
Y J LiDepartment of Anatomy, Norman Bethune College of Medicine, Jilin University, Changchun, China.
E ZacksenhausDepartment of Medicine, University of Toronto, Toronto, Ontario, Canada.
X J HaoState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, PR China.
Y Ben-DavidState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, PR China.
Guiyang Medical University · CNKey Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academy of Sciences · CNFirst Bethune Hospital of Jilin University · CNUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coactosin-like protein (CLP, or Cotl1), is an F-actin-binding protein, whose role in cancer is largely unknown. Here we show that CLP/Cotl1 is highly expressed in a rat epithelial breast cancer cell line (FE1.3) compared with its mesenchymal counterpart (FE1.2). Knockdown of CLP/Cotl1 in FE1.3 cells increased cell proliferation, whereas its overexpression in FE1.2 cells inhibited proliferation in culture and reduced tumor growth in xenograft assays in mice. Mechanistically, we identified two major pathways through which CLP/Cotl1 exerts its suppressive effects. First, CLP/Cotl1 re-expression in FE1.2 and in human MCF7 breast cancer cells induced expression of the growth-suppressor gene interleukin-24 (IL-24), which independently of p53 upregulates the tumor-suppressor genes p53 apoptosis effector related to PMP-22 (PERP) and p21

Indexed as

AnimalsBreast NeoplasmsCarrier ProteinsCyclin-Dependent Kinase Inhibitor p21FemaleGene Knockdown TechniquesGenes, Tumor SuppressorHEK293 CellsHumansInterleukin-24InterleukinsMAP Kinase Signaling SystemMCF-7 CellsMembrane ProteinsMiceMice, Inbred BALB CCarrier ProteinsCDKN1A protein, humanCOTL1 protein, humanCotl1 protein, ratCyclin-Dependent Kinase Inhibitor p21F-actin-binding proteinsInterleukin-24InterleukinsMembrane ProteinsMicrofilament ProteinsPERP protein, humanRNA, Small InterferingTGFB1 protein, humanTgfb1 protein, ratTransforming Growth Factor beta1

Identifiers

PMID28925397
OpenAlexW2754686479

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.