Evidence map›Paper›PMID 29844309›Full record

ArticleCell death & disease2018

FSTL1 interacts with VIM and promotes colorectal cancer metastasis via activating the focal adhesion signalling pathway.

Chuansha Gu, Xiaoyan Wang, Ting Long, Xia Wang, Yan Zhong, Yidan Ma, Zhiyan Hu, Zuguo Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  5. The multifaceted roles of the transcriptional coactivator TAZ in extravillous trophoblast development of the human placenta.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  16. Role of follistatin-like protein 1 in liver diseases.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  17. Article
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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

8 authors at 2 institutions in 1 country.

Chuansha GuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xiaoyan WangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Ting LongDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xia WangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yan ZhongDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yidan MaDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Zhiyan HuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. zhenyucai2011@163.com.
Zuguo LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. Lizg@smu.edu.cn.
Key Laboratory of Guangdong Province · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follistatin-like protein 1 (FSTL1) has been reported to have both tumour-promoting and tumour-suppressive characters. However, the role of FSTL1 in colorectal cancer (CRC) remains unclear. Here we showed that FSTL1 expression was significantly up-regulated in CRC tissues compared with the paired normal tissues. In addition, the higher FSTL1 expression was associated with the infiltrating depth, lymph node metastasis and poor prognosis of CRC. Enhanced expression of FSTL1 distinctly increased cell migration and invasion in vitro, as well as promoting liver metastasis of CRC in vivo. Conversely, knockdown of FSTL1 expression significantly repressed invasion and metastasis of CRC. Mechanically, transcription factor Smad3 was involved in FSTL1 protein expression inducing by TGFβ1-Smad2/3 signalling. Furthermore, this effect of FSTL1 in promoting CRC progression was actualised via activating focal adhesions signalling pathway and regulating cytoskeleton rearrangement. We identified VIM, as an interactive protein of FSTL1, participated in FSTL1-mediated aggressive phenotype. We showed the role of FSTL1 in CRC and explored its transcription regulation and downstream signalling molecular mechanisms. In conclusion, our findings suggested that FSTL1 promoted CRC progression and metastasis, making it a novel target for diagnosis and prognostic evaluation of CRC.

Indexed as

Signal TransductionAnimalsBase SequenceCell Line, TumorCell MovementColorectal NeoplasmsCytoskeletonFemaleFocal AdhesionsFollistatin-Related ProteinsHumansMaleMice, Inbred BALB CMice, NudeMiddle AgedNeoplasm InvasivenessFollistatin-Related ProteinsFSTL1 protein, humanSmad3 ProteinVimentinVIM protein, human

Identifiers

PMID29844309
PMCPMC5974179
OpenAlexW2806746294

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.