Evidence map›Paper›PMID 36690663›Full record

ArticleCell death & disease2023

PTK6 inhibits autophagy to promote uveal melanoma tumorigenesis by binding to SOCS3 and regulating mTOR phosphorylation.

Bo Liu, Xueting Yao, Chaoyang Zhang, Yufen Liu, Li Wei, Qinying Huang, Mengting Wang, Yanchen Zhang, Danning Hu, Wencan Wu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. The multiple roles of autophagy in uveal melanoma and the microenvironment.Journal of cancer research and clinical oncology · 2024
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. The Roles of PTEN in Melanoma Suppression.Pigment cell & melanoma research · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Bioinformatics-based prognostic value andFrontiers in oncology · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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

10 authors at 4 institutions in 2 countries.

Bo LiuState Key Laboratory of Ophthalmology, Optometry and Vision Science, Wenzhou Medical University, Wenzhou, China.
Xueting YaoDepartment of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Chaoyang ZhangDepartment of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Yufen LiuState Key Laboratory of Ophthalmology, Optometry and Vision Science, Wenzhou Medical University, Wenzhou, China.
Li WeiState Key Laboratory of Ophthalmology, Optometry and Vision Science, Wenzhou Medical University, Wenzhou, China.
Qinying HuangState Key Laboratory of Ophthalmology, Optometry and Vision Science, Wenzhou Medical University, Wenzhou, China.
Mengting WangState Key Laboratory of Ophthalmology, Optometry and Vision Science, Wenzhou Medical University, Wenzhou, China.
Yanchen ZhangState Key Laboratory of Ophthalmology, Optometry and Vision Science, Wenzhou Medical University, Wenzhou, China.
Danning HuTissue Culture Center, The New York Eye and Ear Infirmary, New York Medical College, Valhalla, New York, USA.
Wencan WuState Key Laboratory of Ophthalmology, Optometry and Vision Science, Wenzhou Medical University, Wenzhou, China. wuwencan1138@163.com.ORCID 0000-0002-6229-373X
Wenzhou Medical University · CNAnhui Medical University · CNNew York Medical College · USShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy dysfunction is one of the common causes of tumor formation and plays an important role in uveal melanoma (UM). However, little is known about the regulatory mechanisms of autophagy in UM. Here, we show that PTK6 can promote the proliferation, migration, and invasion of UM cells by inhibiting autophagy. SOCS3 can inhibit the proliferation, migration, and invasion of UM cells. Overexpression of SOCS3 can partially rescue the PTK6-induced promotion of UM cell proliferation, migration, and invasion. Mechanistically, PTK6 can bind to SOCS3, and SOCS3 can downregulate the expression of PTK6. Furthermore, PTK6 can upregulate the phosphorylation of mTOR to inhibit autophagy. Taken together, our findings demonstrate the functions of PTK6 and SOCS3 in UM cells and targeting the SOCS3-PTK6 signaling axis might be a novel and promising therapeutic strategy for patients with UM.

Indexed as

ApoptosisCell Transformation, NeoplasticAutophagyCarcinogenesisCell Line, TumorCell MovementCell ProliferationHumansMelanomaNeoplasm ProteinsPhosphorylationProtein-Tyrosine KinasesSuppressor of Cytokine Signaling 3 ProteinTOR Serine-Threonine KinasesUveal MelanomaUveal NeoplasmsMTOR protein, humanNeoplasm ProteinsProtein-Tyrosine KinasesPTK6 protein, humanSOCS3 protein, humanSuppressor of Cytokine Signaling 3 ProteinTOR Serine-Threonine Kinases

Identifiers

PMID36690663
PMCPMC9870980
OpenAlexW4317751994

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.