Evidence map›Paper›PMID 37523636›Full record

ArticleEpigenetics2023

Oncogenic DNA methyltransferase 1 activates the PI3K/AKT/mTOR signalling by blocking the binding of HSPB8 and BAG3 in melanoma.

Yemei Yang, Shengfang Ma, Zi Ye, Yushi Zheng, Zhenjiong Zheng, Xiongshan Liu, Xianyi Zhou

Open access · diamondAbstract read
In one paragraph

Article in Epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Metabolic Reprogramming in Melanoma: An Epigenetic Point of View.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. 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

7 authors at 3 institutions in 2 countries.

Yemei YangDepartment of Dermatology and Venerology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P. R. China.
Shengfang MaDepartment of Dermatology, Baoshihua Hospital of Gansu Province, Lanzhou, P. R. China.
Zi YeCollege of Information and Sciences, The Pennsylvania State University, University of Pennsylvania, Philadelphia, USA.
Yushi ZhengDepartment of Dermatology and Venerology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P. R. China.
Zhenjiong ZhengDepartment of Dermatology and Venerology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P. R. China.
Xiongshan LiuDepartment of Dermatology and Venerology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P. R. China.
Xianyi ZhouDepartment of Dermatology and Venerology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P. R. China.
Third Affiliated Hospital of Southern Medical University · CNDahua Hospital · CNPennsylvania State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal DNA methylation has been observed in multiple malignancies, including melanoma. In this study, we initially noticed the overexpression of DNA methyltransferase 1 (DNMT1) in melanoma samples in bioinformatics analysis and, subsequently, validated it in the purchased melanoma cell lines. After treatment with short-hairpin RNAs or Decitabine (a DNA methylation inhibitor), silencing of DNMT1 was demonstrated to suppress cell viability and invasive and migratory potentials as well as to augment apoptosis and autophagy in melanoma cells. To further explore the downstream mechanisms, we revealed that DNMT1 inhibited HSPB8 expression through augmenting HSPB8 methylation, thereby suppressing the binding between HSPB8 and BAG3. Then, we elucidated through a series of gain- and loss- of function assays that the interplay of HSPB8 and BAG3 blocked the PI3K/AKT/mTOR pathway, thereby repressing the malignant phenotypes of melanoma cells and contributing to melanoma cell apoptosis and autophagy. We further established a mouse model of melanoma and substantiated that DNMT1 enhanced the

Indexed as

MelanomaProto-Oncogene Proteins c-aktAdaptor Proteins, Signal TransducingAnimalsApoptosisApoptosis Regulatory ProteinsAutophagyDNADNA MethylationHeat-Shock ProteinsMethyltransferasesMiceMolecular ChaperonesPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesTOR Serine-Threonine KinasesAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsDNAHeat-Shock ProteinsMethyltransferasesMolecular ChaperonesPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesApoptosisAutophagyBcl2-associated athanogene 3DNA methyltransferase 1Heat shock protein B8MelanomaPI3K/AKT/mTOR pathway

Identifiers

PMID37523636
PMCPMC10392740
OpenAlexW4385409399

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.