Evidence map›Paper›PMID 28815470›Full record

ArticlePathology oncology research : POR2018

Alterations in SCAI Expression during Cell Plasticity, Fibrosis and Cancer.

Ákos Gasparics, Gábor Kökény, Attila Fintha, Rita Bencs, Miklós M Mózes, Emese Irma Ágoston, Anna Buday, Zoltán Ivics, Péter Hamar, Balázs Győrffy and 2 more

Abstract read
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In one paragraph

Article in Pathology oncology research : POR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Bridging Gaps in HDR Improvement: The Role of MAD2L2, SCAI, and SCR7.International journal of molecular sciences · 2023
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Oncogenic microRNA-1290 andTechnology in cancer research & treatment
    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

12 authors at 2 institutions in 2 countries.

Ákos GasparicsDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary.
Gábor KökényDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary.
Attila Fintha2nd Department of Pathology, Semmelweis University, Budapest, Hungary.
Rita BencsDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary.
Miklós M MózesDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary.
Emese Irma Ágoston1st Department of Surgery, Semmelweis University, Budapest, Hungary.
Anna BudayDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary.
Zoltán IvicsDivision of Medical Biotechnology, Paul Ehrlich Institute, Langen, Germany.
Péter HamarDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary.
Balázs GyőrffyMTA TTK Lendület Cancer Biomarker Research Group, Budapest, Hungary.
László RosivallDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary.
Attila SebeDepartment of Pathophysiology, Semmelweis University, Nagyvarad ter 4, rm 1810, Budapest, 1089, Hungary. sebe.attila@med.semmelweis-univ.hu.ORCID http://orcid.org/0000-0001-7814-5144
Semmelweis University · HUPaul Ehrlich Institut · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Suppressor of cancer cell invasion (SCAI) has been originally characterized as a tumor suppressor inhibiting metastasis in different human cancer cells, and it has been suggested that SCAI expression declines in tumors. The expression patterns and role of SCAI during physiological and pathophysiological processes is still poorly understood. Earlier we demonstrated that SCAI is regulating the epithelial-mesenchymal transition of proximal tubular epithelial cells, it is downregulated during renal fibrosis and it is overexpressed in Wilms' tumors. Here we bring further evidence for the involvement of SCAI during cell plasticity and we examine the prognostic value and expression patterns of SCAI in various tumors. SCAI prevented the activation of the SMA promoter induced by angiotensin II. SCAI expression decreased in a model of endothelial-mesenchymal transition and increased during iPS reprogramming of fibroblasts. During renal fibrosis SCAI expression declined, as evidenced in a rat model of renal transplant rejection and in TGF-β1 overexpressing transgenic mice. High expression of SCAI correlated with better survival in patients with breast and lung cancers. Intriguingly, in the case of other cancers (gastric, prostate, colorectal) high SCAI expression correlated with poor survival of patients. Finally, we bring evidence for SCAI overexpression in colorectal cancer patients, irrespective of stage or metastatic status of the disease, suggesting a diverse role of SCAI in various diseases and cancer.

Indexed as

Cell PlasticityAgedAged, 80 and overAnimalsBiomarkersBreast NeoplasmsCase-Control StudiesCells, CulturedColorectal NeoplasmsEpithelial-Mesenchymal TransitionFemaleFibrosisFollow-Up StudiesHumansHuman Umbilical Vein Endothelial CellsKidney DiseasesBiomarkersSCAI protein, humanTranscription FactorsCancerCell plasticityEpithelial-mesenchymal transition (EMT)FibrosisSuppressor of cancer cell invasion (SCAI)

Identifiers

PMID28815470
OpenAlexW2748983793

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.