Evidence map›Paper›PMID 27276686›Full record

ArticleOncotarget2016

ATG4A promotes tumor metastasis by inducing the epithelial-mesenchymal transition and stem-like properties in gastric cells.

Shi-Wei Yang, Yi-Fang Ping, Yu-Xing Jiang, Xiao Luo, Xia Zhang, Xiu-Wu Bian, Pei-Wu Yu

RetractedOpen access · diamondAbstract readRetracted Publication
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Autophagy Protease ATG4D Facilitates Proliferation and Malignancy of Osteosarcoma Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  2. Article
  3. Role of Tumor Cell Intrinsic and Host Autophagy in Cancer.Cold Spring Harbor perspectives in medicine · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Shi-Wei YangDepartment of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Yi-Fang PingKey Laboratory of Tumor Immunopathology of Ministry of Education of China, Third Military Medical University, Chongqing, China.
Yu-Xing JiangDepartment of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xiao LuoDepartment of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xia ZhangKey Laboratory of Tumor Immunopathology of Ministry of Education of China, Third Military Medical University, Chongqing, China.
Xiu-Wu BianKey Laboratory of Tumor Immunopathology of Ministry of Education of China, Third Military Medical University, Chongqing, China.
Pei-Wu YuDepartment of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Southwest Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The metastasis of tumor cells to distant organs is an ominous feature of gastric cancer. However, the molecular mechanisms underlying the invasion and metastasis of gastric cancer cells remain elusive. In this study, we found that the expression of ATG4A, an autophagy-regulating molecule, was significantly increased in gastric cancer tissues and was significantlycorrelated with the gastric cancer differentiation degree, tumor invasion and lymph node metastasis. ATG4A over-expression significantly promoted gastric cancer cell migration and invasion in vitro and metastasis in vivo, as well as promoted gastric cancer cell stem-like properties and the epithelial-mesenchymal transition (EMT) phenotype. By contrast, ATG4A knockdown inhibited the migration, invasion and metastasis of cancer cells, as well as the stem-like properties and EMT phenotype. Mechanistically, ATG4A promotes gastric cancer cell stem-like properties and the EMT phenotype through the activation of Notch signaling not via autophagy, and using the Notch signaling inhibitor DAPT attenuated the effects of ATG4A on gastric cancer cells. Taken together, these findings demonstrated that ATG4A promotes the metastasis of gastric cancer cells via the Notch signaling pathway, which is an autophagy-independent mechanism.

Indexed as

Epithelial-Mesenchymal TransitionAgedAnimalsAutophagy-Related ProteinsCell DifferentiationCell Line, TumorCell MovementCell ProliferationCysteine EndopeptidasesFemaleHumansLymphatic MetastasisMaleMiceMice, NudeMiddle AgedATG4A protein, humanAutophagy-Related ProteinsCysteine EndopeptidasesProto-Oncogene Proteins c-aktVimentinATG4Aepithelial-mesenchymal transitiongastric cancermetastasisPathology Sectiontumor stem cell

Identifiers

PMID27276686
PMCPMC5129932
OpenAlexW2418167488

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.