Evidence map›Paper›PMID 29115636›Full record

ArticleOncology reports2018

FSTL1 suppresses tumor cell proliferation, invasion and survival in non-small cell lung cancer.

Xiaolei Ni, Xiaoming Cao, Yongquan Wu, Jian Wu

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. CD11bAmerican journal of cancer research · 2021
    Article
  11. FSTL-1 Attenuation Causes Spontaneous Smoke-Resistant Pulmonary Emphysema.American journal of respiratory and critical care medicine · 2020
    Article
  12. FSTL-1: A New Player in the Prevention of Emphysema.American journal of respiratory and critical care medicine · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Follistatin-like 1 in development and human diseases.Cellular and molecular life sciences : CMLS · 2018
    Review
  18. Oncology letters · 2018
    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

4 authors at 2 institutions in 1 country.

Xiaolei NiDepartment of Medical Oncology, The First Hospital of Longyan Affiliated to Fujian Medical University, Longyan, Fujian, P.R. China.
Xiaoming CaoDepartment of Respiratory Medicine, The First Hospital of Longyan Affiliated to Fujian Medical University, Longyan, Fujian, P.R. China.
Yongquan WuDepartment of Respiratory Medicine, The First Hospital of Longyan Affiliated to Fujian Medical University, Longyan, Fujian, P.R. China.
Jian WuDepartment of Cardiothoracic Surgery, The First Hospital of Longyan Affiliated to Fujian Medical University, Longyan, Fujian, P.R. China.
Fujian Medical University · CNFirst Affiliated Hospital of Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follistatin like-1 (FSTL1) is a secreted glycoprotein involved in a series of physiological and pathological processes. However, its contribution to the development of cancer, especially the pathogenesis of NSCLC, remains to be elucidated. We explored the expression, function, and molecular mechanism of FSTL1 in NSCLC. In this study, we detected the expression of FSTL1 in a panel of NSCLC cell lines and lung normal epithelial cell line by qRT-PCR and western blot analysis and found that FSTL1 was downregulated in NSCLC cells compared with normal control. Knockdown of FSTL1 with different shRNA sequences result in increased cell proliferation and cell migration, invasion and reduced cell apoptosis in A549 cell line with high FSTL1 endogenous level. FSTL1 overexpression in H446 cell line with low FSTL1 endogenous level suppressed cell proliferation and migration, invasion and increased cell apoptosis. Knockdown and overexpression of FSTL1 caused altered cell cycle. Reduced cell apoptosis was revealed in FSTL1 knockdown cells accompanied by increased FAS expression and decreased FASL, cleaved caspase‑3 and ‑7 expression. By contrast, overexpression of FSTL1 caused reduced FAS level and increased activated caspase‑3 and ‑7 expression, which may lead to increased cell apoptosis. Moreover, the changed migration and invasion ability in FSTL1 sufficient or deficient cells may be caused by alterations in MMP2, MMP3 and MMP9 expression. Altogether, our results revealed the critical tumor-suppression function of FSTL1 in NSCLC progression, suggesting that FSTL1 might be an important factor in NSCLC progression.

Indexed as

A549 CellsCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell MovementCell ProliferationDown-RegulationFollistatin-Related ProteinsGene Expression Regulation, NeoplasticHumansLung NeoplasmsNeoplasm InvasivenessFollistatin-Related ProteinsFSTL1 protein, human

Identifiers

PMID29115636
PMCPMC5783594
OpenAlexW2765575304

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.