Evidence map›Paper›PMID 40148689›Full record

ArticleOncogene2025

SUMOylation facilitates the stability of BCR-ABL to promote chronic myeloid leukemia progression.

Lu Zhang, Xuefeng Wang, Dongmei Hu, Shijie Li, Mingshan Sun, Qian Liu, Huimin Feng, Minran Zhou, Chunyan Chen, Huan Zhou and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

11 authors.

Lu ZhangDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xuefeng WangNational Drug Clinical Trial Institution, the First Affiliated Hospital of Bengbu Medical University, Bengbu, China.
Dongmei HuDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Shijie LiDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Mingshan SunDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Qian LiuDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Huimin FengDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Minran ZhouDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Chunyan ChenDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China. chency@sdu.edu.cn.ORCID http://orcid.org/0000-0002-5919-7624
Huan ZhouNational Drug Clinical Trial Institution, the First Affiliated Hospital of Bengbu Medical University, Bengbu, China. zhouhuan@bbmc.edu.cn.ORCID http://orcid.org/0000-0002-7316-8467
Sai MaDepartment of Hematology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China. masai@qiluhospital.com.ORCID http://orcid.org/0000-0002-1435-6716

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82070164National Natural Science Foundation of China (National Science Foundation of China) 82300188
6 · The paper itself

Abstract

Tyrosine kinase inhibitors (TKIs) targeting the oncoprotein BCR-ABL have improved the prognosis for patients with chronic myeloid leukemia (CML). However, TKI resistance and persistent expression of BCR-ABL are responsible for the relapse and progression of CML. Here, we describe a novel approach to induce BCR-ABL protein degradation by small ubiquitin-like modifier (SUMO) modification. The E3 SUMO ligase TRIM28, upregulated during the progression of CML, promoted SUMOylation of BCR-ABL, thereby inhibiting its binding to the autophagy receptor P62 and repressing its autophagic degradation. Accordingly, genetic and pharmacological inhibition of TRIM28 or SUMOylation suppressed progression in both the CML mouse model and patient-derived xenograft model. Furthermore, targeting SUMOylation of BCR-ABL restrained the proliferation of TKI-resistant CML cells. These results identify the mechanism by which TRIM28 maintains BCR-ABL stability to promote CML progression and suggest SUMOylation as a target for CML treatment.

Indexed as

Fusion Proteins, bcr-ablLeukemia, Myelogenous, Chronic, BCR-ABL PositiveSumoylationTripartite Motif-Containing Protein 28AnimalsCell Line, TumorCell ProliferationDisease ProgressionDrug Resistance, NeoplasmHumansMiceProtein Kinase InhibitorsProtein StabilityXenograft Model Antitumor AssaysFusion Proteins, bcr-ablProtein Kinase InhibitorsTRIM28 protein, humanTripartite Motif-Containing Protein 28

Identifiers

PMID40148689

What OpenQuestion holds

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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.