Evidence map›Paper›PMID 40097917›Full record

ArticleAutophagy2025

H3K36me2 methyltransferase NSD2/WHSC1 promotes triple-negative breast cancer metastasis via activation of ULK1-dependent autophagy.

Danyang Chen, Xiaohui Chen, Mingqiang Yang, Qiunuo Li, Shaojuan Weng, Siyue Kou, Xi Liu, Guanmin Jiang, Hao Liu

Abstract read
In one paragraph

Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Ultrasound-activated CuJournal of nanobiotechnology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Many faces of mammalian NSD methyltransferases.Cellular & molecular biology letters · 2026
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. 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

9 authors.

Danyang ChenGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.ORCID 0000-0002-7894-9457
Xiaohui ChenDepartment of Clinical Laboratory, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong, China.ORCID 0009-0008-2181-7630
Mingqiang YangGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Qiunuo LiDepartment of Clinical Laboratory, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong, China.
Shaojuan WengGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Siyue KouGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Xi LiuThe Molecular Diagnosis Center, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University Peking University Cancer Hospital, Kunming, Yunnan, China.ORCID 0009-0009-2187-3488
Guanmin JiangDepartment of Clinical Laboratory, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong, China.ORCID 0000-0002-0397-1860
Hao LiuGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.ORCID 0000-0002-9797-2011

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is the primary cause for treatment failure and poor prognosis in patients with triple-negative breast cancer (TNBC). Macroautophagy/autophagy plays a crucial role in tumor growth and metastasis. Genetic or epigenetic regulation of autophagy-related factors alters autophagy levels, which subsequently promotes cancer progression and affects the therapeutic effectiveness. However, the molecular basis for the transcriptional and epigenetic regulation of autophagy in TNBC progression is poorly understood. In this study, we reveal the histone methyltransferase NSD2/WHSC1 (nuclear receptor binding SET domain protein 2) as a novel epigenetic regulator of autophagy in TNBC progression. We demonstrate that the expression of NSD2 is significantly upregulated in TNBC cells and high NSD2 expression is correlated with poor TNBC survival. Elevated expression of NSD2 significantly promotes TNBC metastasis in multiple TNBC models. Mechanistically, ULK1 (unc-51 like autophagy activating kinase 1) is identified as a novel target of NSD2 and NSD2-mediated histone H3K36me2 methylation directly activates ULK1 transcription in TNBC cells. Notably, NSD2-induced ULK1 expression facilitates autophagosome maturation and increases autophagic flux, thus promoting autophagy-related malignancy progression in TNBC. Furthermore, pharmacological inhibition of NSD2 using MS159 and MCTP-39 significantly suppresses TNBC autophagy, growth, and metastasis both

Indexed as

AutophagyAutophagy-Related Protein-1 HomologHistone-Lysine N-MethyltransferaseHistonesIntracellular Signaling Peptides and ProteinsRepressor ProteinsTriple Negative Breast NeoplasmsAnimalsCell Line, TumorEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHumansMethylationMiceMice, NudeAutophagy-Related Protein-1 HomologHistone-Lysine N-MethyltransferaseHistonesIntracellular Signaling Peptides and ProteinsNSD2 protein, humanRepressor ProteinsULK1 protein, humanAutophagyH3K36me2metastasisNSD2triple-negative breast cancerULK1

Identifiers

PMID40097917
PMCPMC12283020

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Registered trials

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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.