Evidence map›Paper›PMID 38822351›Full record

ArticleMolecular cancer2024

N6-methyladenosine-modified SENP1, identified by IGF2BP3, is a novel molecular marker in acute myeloid leukemia and aggravates progression by activating AKT signal via de-SUMOylating HDAC2.

Diguang Wen, Hang Xiao, Yueyi Gao, Hanqing Zeng, Jianchuan Deng

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Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

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40citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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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

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3 · Its place in the literature

Who cites it

40 citing papers in PubMed.

  1. METTL16 S-glutathionylation-triggered RNA mActa pharmacologica Sinica · 2026
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  11. Translational cancer research · 2026
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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Diguang WenDepartment of Hematology, Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Hang XiaoDepartment of Hematology, Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Yueyi GaoDepartment of Hematology, Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Hanqing ZengDepartment of Hematology, Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. 233318983@qq.com.
Jianchuan DengDepartment of Hematology, Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. dengjianchuan66@163.com.

Funding

the Natural Science Foundation of Chongqing, China 2021jcyj-msxmX0064
6 · The paper itself

Abstract

backgroundElevated evidence suggests that the SENPs family plays an important role in tumor progression. However, the role of SENPs in AML remains unclear.

methodsWe evaluated the expression pattern of SENP1 based on RNA sequencing data obtained from OHSU, TCGA, TARGET, and MILE datasets. Clinical samples were used to verify the expression of SENP1 in the AML cells. Lentiviral vectors shRNA and sgRNA were used to intervene in SENP1 expression in AML cells, and the effects of SENP1 on AML proliferation and anti-apoptosis were detected using in vitro and in vivo models. Chip-qPCR, MERIP-qPCR, CO-IP, RNA pulldown, and dual-luciferase reporter gene assays were used to explore the regulatory mechanisms of SNEP1 in AML.

resultsSENP1 was significantly upregulated in high-risk AML patients and closely related to poor prognosis. The AKT/mTOR signaling pathway is a key downstream pathway that mediates SENP1's regulation of AML proliferation and anti-apoptosis. Mechanistically, the CO-IP assay revealed binding between SENP1 and HDAC2. SUMO and Chip-qPCR assays suggested that SENP1 can desumoylate HDAC2, which enhances EGFR transcription and activates the AKT pathway. In addition, we found that IGF2BP3 expression was upregulated in high-risk AML patients and was positively correlated with SENP1 expression. MERIP-qPCR and RIP-qPCR showed that IGF2BP3 binds SENP1 3-UTR in an m6A manner, enhances SENP1 expression, and promotes AKT pathway conduction.

conclusionsOur findings reveal a distinct mechanism of SENP1-mediated HDAC2-AKT activation and establish the critical role of the IGF2BP3/SENP1signaling axis in AML development.

Indexed as

AdenosineCell ProliferationCysteine EndopeptidasesHistone Deacetylase 2Leukemia, Myeloid, AcuteProto-Oncogene Proteins c-aktRNA-Binding ProteinsSumoylationAnimalsApoptosisBiomarkers, TumorCell Line, TumorDisease ProgressionFemaleGene Expression Regulation, LeukemicHumansAdenosineBiomarkers, TumorCysteine EndopeptidasesHDAC2 protein, humanHistone Deacetylase 2IGF2BP3 protein, humanN-methyladenosineProto-Oncogene Proteins c-aktRNA-Binding ProteinsSENP1 protein, humanAcute myeloid leukemiam6ASENP1SUMO

Identifiers

PMID38822351
PMCPMC11141000

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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.