Evidence map›Paper›PMID 27181092›Full record

ArticleScientific reports2016

LASP1-S100A11 axis promotes colorectal cancer aggressiveness by modulating TGFβ/Smad signaling.

Ya Niu, Ziyun Shao, Hui Wang, Jiaqi Yang, Feifei Zhang, Yuhao Luo, Lijun Xu, Yanqing Ding, Liang Zhao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. The roles of FLOT1 in human diseases (Review).Molecular medicine reports · 2023
    Review
  11. Article
  12. Review
  13. Gene network revealsFrontiers in neurology · 2023
    Article
  14. Article
  15. Article
  16. Review
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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 1 country.

Ya NiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ziyun ShaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Hui WangDepartment of Medical Oncology, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Jiaqi YangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Feifei ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yuhao LuoDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Lijun XuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yanqing DingDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Liang ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Southern Medical University · CNNanfang Hospital · CNGuangzhou Medical University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LIM and SH3 protein 1(LASP1) can promote colorectal cancer (CRC) progression and metastasis, but the mechanism remains unclear. Here, we show that LASP1 interacts with S100 calcium binding protein A11(S100A11) and enhances its expression in CRC. LASP1-S100A11 axis is essential for TGFβ-mediated epithelial-mesenchymal transition (EMT) and cell aggressive phenotype. Clinically, S100A11 is overexpressed in CRC tissues and localized in both the cytoplasm and the nucleus of CRC cells. Overexpression of S100A11 in cytoplasmic and nuclear subcellular compartments is associated with tumor metastasis and poor prognosis of CRC patients. Introduction of cytoplasmic and nuclear S100A11 promotes aggressive phenotypes of CRC cells in vitro as well as growth and metastasis of CRC xenografts, whereas suppressing S100A11 abrogates these effects. Furthermore, we identify flotillin-1 (FLOT1) and histone H1 as downstream factors for cytoplasmic and nuclear pathway of S100A11, which are required for LASP1-S100A11 axis-mediated EMT and CRC progression. These findings indicate S100A11, combined with LASP1, plays a critical role in promoting CRC metastasis via its subcellular effectors, FLOT1 and histone H1.

Indexed as

Epithelial-Mesenchymal TransitionSignal TransductionAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorCell NucleusColorectal NeoplasmsCytoplasmCytoskeletal ProteinsHeterograftsHumansLIM Domain ProteinsMembrane ProteinsMiceNeoplasm TransplantationS100 ProteinsAdaptor Proteins, Signal TransducingCytoskeletal ProteinsflotillinsLASP1 protein, humanLIM Domain ProteinsMembrane ProteinsS100A11 protein, humanS100 ProteinsTransforming Growth Factor beta

Identifiers

PMID27181092
PMCPMC4867635
OpenAlexW2398161251

What OpenQuestion holds

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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.