Evidence map›Paper›PMID 30832706›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

FAT4 regulates the EMT and autophagy in colorectal cancer cells in part via the PI3K-AKT signaling axis.

Ran Wei, Yuhong Xiao, Yi Song, Huiping Yuan, Jun Luo, Wei Xu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
19.8field-weighted citation impact, top 1% 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

112 citing papers in PubMed, 217 citations in OpenAlex.

  1. Article
  2. FAT4 loss promotes tumor growth and ferroptosis resistance in hepatocellular carcinoma via PI3K/AKT pathway activation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

52 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Ran WeiThe First Clinical Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China.
Yuhong XiaoDepartment of Rehabilitation Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Yi SongDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Huiping YuanDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Jun LuoDepartment of Rehabilitation Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China. luojun1786@163.com.
Wei XuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China. xu_wei111@126.com.
Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CN

Funding

National Natural Science Foundation of China 81560365National Natural Science Foundation of China 81760408National Natural Science Foundation of China 81860435
6 · The paper itself

Abstract

backgroundFAT4 functions as a tumor suppressor, and previous findings have demonstrated that FAT4 can inhibit the epithelial-to-mesenchymal transition (EMT) and the proliferation of gastric cancer cells. However, few studies have investigated the role of FAT4 in the development of colorectal cancer (CRC). The current study aimed to detect the role of FAT4 in the invasion, migration, proliferation and autophagy of CRC and elucidate the probable molecular mechanisms through which FAT4 interacts with these processes.

methodsTranswell invasion assays, MTT assays, transmission electron microscopy, immunohistochemistry and western blotting were performed to evaluate the migration, invasion, proliferation and autophagy abilities of CRC cells, and the levels of active molecules involved in PI3K/AKT signaling were examined through a western blotting analysis. In addition, the function of FAT4 in vivo was assessed using a tumor xenograft model.

resultsFAT4 expression in CRC tissues was weaker than that in nonmalignant tissues and could inhibit cell invasion, migration, and proliferation by promoting autophagy in vitro. Furthermore, the regulatory effects of FAT4 on autophagy and the EMT were partially attributed to the PI3K-AKT signaling pathway. The results in vivo also showed that FAT4 modulated CRC tumorigenesis.

conclusionFAT4 can regulate the activity of PI3K to promote autophagy and inhibit the EMT in part through the PI3K/AKT/mTOR and PI3K/AKT/GSK-3β signaling pathways.

Indexed as

AnimalsAutophagyCadherinsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansMiceNeoplasm InvasivenessPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCadherinsFAT4 protein, humanGlycogen Synthase Kinase 3 betaMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTumor Suppressor ProteinsAutophagyColorectal cancerEMTFAT4PI3K/AKTProliferation

Identifiers

PMID30832706
PMCPMC6399964
OpenAlexW2942596637

What OpenQuestion holds

Textmetadata
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.