Related Experiment Video

Updated: Jan 12, 2026

Three Dimensional Cultures: A Tool To Study Normal Acinar Architecture vs. Malignant Transformation Of Breast Cells
08:33

Three Dimensional Cultures: A Tool To Study Normal Acinar Architecture vs. Malignant Transformation Of Breast Cells

Published on: April 25, 2014

20.3K

Targeting the N-cadherin/β-catenin axis with MSAB reverses malignant phenotypes in blast crisis of CML

Yingying Zhou1, Songqin Jian2, Lijun Lu1

  • 1Department of Laboratory Medicine, Huangyan Hospital of Wenzhou Medical University, Taizhou First People's Hospital, Taizhou, Zhejiang, China.

Frontiers in Oncology
|November 3, 2025
PubMed
Abstract

Insights

N-cadherin (CDH2) drives chronic myeloid leukemia (CML) progression to blast crisis by activating Wnt/β-catenin signaling. Inhibiting this pathway with MSAB offers a potential therapeutic strategy for advanced CML.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Chronic myeloid leukemia (CML) progression from chronic phase (CP) to blast crisis (BC) involves complex molecular mechanisms.
  • Understanding these mechanisms is crucial for developing effective treatments for advanced CML.

Purpose of the Study:

  • Identify genes driving CML progression from CP to BC.
  • Elucidate the specific role of N-cadherin (CDH2) in BC transformation.

Main Methods:

  • Analyzed the GSE4170 dataset for differentially expressed genes (DEGs) in CML phases.
  • Utilized Gene Set Enrichment Analysis (GSEA), Gene Ontology (GO), and KEGG pathway analyses for functional annotation.
  • Validated N-cadherin's role using in vitro (KU812 cells) and in vivo (nude mouse xenograft) models.
  • Investigated mechanisms using the β-catenin inhibitor MSAB.

Main Results:

  • Identified 1,294 DEGs, with 41 progression-specific genes.
  • Found significant upregulation of N-cadherin (CDH2) in BC samples.
  • N-cadherin overexpression promoted cell cycle entry, accelerated tumor growth, and suppressed differentiation.
  • MSAB treatment reversed these malignant phenotypes, indicating CDH2's role via Wnt/β-catenin signaling.

Conclusions:

  • CDH2 plays a critical role in CML progression to BC by activating the Wnt/β-catenin pathway.
  • Targeting the N-cadherin/β-catenin axis with MSAB presents a promising therapeutic strategy for BC-CML.
Keywords:
CML progressionMSABN-cadherinWnt signalingexression profileβ-catenin

More Related Videos

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

14.2K
Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.6K

Related Concept Videos

Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
3.9K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.6K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.1K
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
6.4K