Insufficient microwave ablation-induced promotion of distant metastasis is suppressed by β-catenin pathway inhibition in breast cancer
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Peng Kong1,*, Hong Pan1,*, Muxin Yu1,*, Lie Chen1, Han Ge1, Jin Zhu1, Ge Ma1, Li Li1, Qiang Ding1, Wenbin Zhou1 and Shui Wang1
1Department of Breast Surgery, The First Affiliated Hospital with Nanjing Medical University, 210029 Nanjing, China
*These authors have contributed equally to this work
Shui Wang, email: firstname.lastname@example.org
Wenbin Zhou, email: email@example.com
Keywords: microwave ablation; breast cancer; epithelial-mesenchymal transition (EMT); β-catenin; metastasis
Received: August 30, 2017 Accepted: November 16, 2017 Published: December 01, 2017
Microwave ablation (MWA), a thermal ablation, is an effective treatment for breast cancer. However, residual breast cancer is still detected. The biological characteristics of residual breast cancer after thermal ablation remain unknown. To mimic insufficient MWA in vitro, breast cancer cells were treated at 37°C, 42°C, 45°C, 47°C and 50°C for 10 mins, the 37°C as control group. Insufficient MWA induced EMT-like changes of residual breast cancer by down-regulation of E-cadherin and up-regulation of vimentin and N-cadherin in vitro and in vivo. For the first time, we reported insufficient MWA promoted distant metastasis of residual breast cancer in vivo. Reduced β-catenin expression by siRNA diminished the EMT-like phenotype and enhanced migration capability induced by heat treatment in breast cancer cells. Moreover, ICG001, a special inhibitor of β-catenin pathway, depressed EMT of residual tumor and distant metastasis in an insufficient MWA nude mice model of breast cancer. In conclusion, our results demonstrate that insufficient MWA promotes EMT of residual breast cancer by activating β-catenin signal pathway, resulting in enhanced distant metastasis of residual breast cancer. In addition, the effectiveness of ICG001 in suppressing enhanced metastasis of residual breast cancer is preliminarily validated.
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