Evidence map›Paper›PMID 42145780›Full record

ArticleFrontiers in medicine2026

Dickkopf 2 serves as a novel therapeutic target and prognostic biomarker in acute myeloid leukemia targeted by evodiamine.

Rui Li, Weiguang Jiang, Xiaomei Sun, Yan-Hua Su

Abstract read
In one paragraph

Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

0 citing papers in PubMed.

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4 · The record

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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

4 authors.

Rui Li *Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Weiguang Jiang *The Eighth Orthopedic Ward of Harbin Fifth Hospital Harbin, Heilongjiang, China.
Xiaomei SunDepartment of Gastroenterology, Hospital of Heilongjiang Provincial, Harbin, Heilongjiang, China.
Yan-Hua SuDepartment of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Acute myeloid leukemia (AML) has seen a significant increase in cases recently, often leading to a poor outlook. Dysregulated cell death is a characteristic of AML that aids in both the formation and advancement of the disease. Dickkopf 2 (DKK2) is known to promote tumorigenesis and metastasis through multiple mechanisms, facilitating cancer development and progression. The specific function of DKK2 in AML is not yet completely understood. Materials and methods: The potential of DKK2 as a prognostic marker in AML was assessed using data from the Gene Expression Omnibus (GEO; accession number GSE26294) and The Cancer Genome Atlas (TCGA). Cell growth, proliferation, apoptosis, and migration were assessed following the upregulation or downregulation of DKK2 in AML cells using CCK-8, EdU staining, AO/EB staining, and transwell assays. Furthermore, molecular docking and dynamics simulations were performed to predict the interaction and binding affinity between DKK2 and evodiamine. Rescue experiments were further conducted to elucidate the functional relationship between DKK2 and evodiamine. Results: In AML, DKK2 expression was notably increased and linked to poor overall survival. Reducing DKK2 levels hindered AML cell growth, proliferation, and migration, while promoting apoptosis. Conversely, overexpression of DKK2 promoted the malignant phenotype of AML cells. Additionally, evodiamine was identified as a potential small-molecule compound that may functionally regulate DKK2 in AML evodiamine showed a strong binding affinity to DKK2, with a binding energy measured at -5.51 kcal/mol. Importantly, the overexpression of DKK2 negated the anti-cancer effects of evodiamine in AML cells. Conclusion: The DKK2/evodiamine axis represents a novel prognostic biomarker and a promising therapeutic target for AML.

Indexed as

acute myeloid leukemiaDickkopf 2evodiaminefunctionmolecular docking

Identifiers

PMID42145780
PMCPMC13171552

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