Incomplete radiofrequency ablation enhances invasiveness and metastasis of residual cancer of hepatocellular carcinoma cell HCCLM3 via activating β-catenin signaling.
Incomplete radiofrequency ablation enhances invasiveness and metastasis of residual cancer of hepatocellular carcinoma cell HCCLM3 via activating β-catenin signaling.
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不完全射频消融通过激活β-catenin信号增强肝细胞癌细胞HCCLM3残留癌的侵袭和转移。
DOI：
10.1371/journal.pone.0115949
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Tang ZY
中科院分区：
文献类型：
--
作者：
Zhang N;Wang L;Chai ZT;Zhu ZM;Zhu XD;Ma DN;Zhang QB;Zhao YM;Wang M;Ao JY;Ren ZG;Gao DM;Sun HC;Tang ZY
Radiofrequency ablation (RFA) is one of the curative therapies for hepatocellular carcinoma (HCC), however, accelerated progression of residual HCC after incomplete RFA has been reported more frequently. The underlying molecular mechanism of this phenomenon remains to be elucidated. In this study, we used an incomplete RFA orthotopic HCC nude mouse model to study the invasive and metastatic potential of residual cancer as well as the correlated mechanism. The incomplete RFA orthotopic nude mouse models were established using high metastatic potential HCC cell line HCCLM3 and low metastatic potential HCC cell line HepG2, respectively. The changes in cellular morphology, motility, metastasis and epithelial–mesenchymal transition (EMT), and HCC cell molecular markers after in vitro and in vivo incomplete RFA intervention were observed. Pulmonary and intraperitoneal metastasis were observed in an in vivo study. The underlying pro-invasive mechanism of incomplete RFA appeared to be associated with promoting EMT, including down-regulation of E-cadherin and up-regulation of N-cadherin and vimentin. These results were in accordance with the in vitro response of HCC cells to heat intervention. Further studies demonstrated that β-catenin was a pivotal factor during this course and blocking β-catenin reduced metastasis and EMT phenotype changes in heat-treated HCCLM3 cells in vitro. Incomplete RFA enhanced the invasive and metastatic potential of residual cancer, accompanying with EMT-like phenotype changes by activating β-catenin signaling in HCCLM3 cells.
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影响因子：
13.5
作者：
Llovet, Josep M.;Bruix, Jordi
通讯作者：
Bruix, Jordi
影响因子：
24.5
作者：
Hur K;Toiyama Y;Takahashi M;Balaguer F;Nagasaka T;Koike J;Hemmi H;Koi M;Boland CR;Goel A
通讯作者：
Goel A
影响因子：
3.3
作者：
Medici, Damian;Hay, Elizabeth D.;Olsen, Bjorn R.
通讯作者：
Olsen, Bjorn R.
影响因子：
7.3
作者：
Oh, Seo Jin;Shin, Jung-Ho;Kim, Tae Hoon;Lee, Hee Sun;Yoo, Jung-Yoon;Ahn, Ji Yeon;Broaddus, Russell R.;Taketo, Makoto M.;Lydon, John P.;Leach, Richard E.;Lessey, Bruce A.;Fazleabas, Asgerally T.;Lim, Jeong Mook;Jeong, Jae-Wook
通讯作者：
Jeong, Jae-Wook
影响因子：
254.7
作者：
Parkin, DM;Bray, F;Pisani, P
通讯作者：
Pisani, P