Interaction Between Wnt/β-catenin Signaling Pathway and EMT Pathway Mediates the Mechanism of Sunitinib Resistance in Renal Cell Carcinoma
Overview
Affiliations
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.
Gan W, Chen C, Huang M, Li Y Oncol Lett. 2024; 28(6):560.
PMID: 39372664 PMC: 11450707. DOI: 10.3892/ol.2024.14693.
MAP7 drives EMT and cisplatin resistance in ovarian cancer via wnt/β-catenin signaling.
Chen Q, Li S, Fu F, Huang Q, Zhang R Heliyon. 2024; 10(9):e30409.
PMID: 38726137 PMC: 11078642. DOI: 10.1016/j.heliyon.2024.e30409.