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Interaction Between Wnt/β-catenin Signaling Pathway and EMT Pathway Mediates the Mechanism of Sunitinib Resistance in Renal Cell Carcinoma

Overview
Journal BMC Cancer
Publisher Biomed Central
Specialty Oncology
Date 2024 Feb 5
PMID 38317072
Authors
Affiliations
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Abstract

Background: Targeted drugs are the main methods of RCC treatment. However, drug resistance is common in RCC patients, in-depth study of the drug-resistant mechanism is essential.

Methods: We constructed sunitinib resistant and Twist overexpressed A498 cells, and studied its mechanisms in vitro and in vivo.

Results: In cell research, we found that either sunitinib resistance or Twist overexpression can activate Wnt/β-catenin and EMT signaling pathway, and the sunitinib resistance may work through β-catenin/TWIST/TCF4 trimer. In zebrafish research, we confirmed the similarity of Twist overexpression and sunitinib resistance, and the promoting effect of Twist overexpression on drug resistance.

Conclusions: Sunitinib resistance and Twist overexpression can activate Wnt/β-catenin signaling pathway and EMT to promote the growth and metastasis of RCC cells.

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