scholarly journals Establishment of an insufficient radiofrequency ablation orthotopic nude mouse model of hepatocellular carcinoma to study the invasiveness and metastatic potential of residual cancer

2019 ◽  
Author(s):  
Ning Zhang ◽  
Hua Zhu ◽  
Ye‑Hao Dong ◽  
Lu Wang
2018 ◽  
Vol 17 (4) ◽  
pp. 1260-1269
Author(s):  
Ning Zhang ◽  
Long-Rong Wang ◽  
Dou-Dou Li ◽  
De-Ning Ma ◽  
Cheng-Hao Wang ◽  
...  

Objective: We had previously proved that insufficient radiofrequency ablation (RFA) could enhance invasiveness and metastasis of hepatocellular carcinoma (HCC) through epithelial-mesenchymal transition (EMT), which is mediated by activating β-catenin signaling. Thus, the aim of the present study was to demonstrate whether the combined treatment of interferon-α (IFN-α) and “Songyou Yin” (SYY) minimizes the pro-metastatic effects of insufficient RFA, as well as to explore its underlying mechanism. Methods: Insufficient RFA was performed in an orthotopic nude mice model of HCCLM3 with high metastatic potential. The effects of IFN-α, SYY, and combined IFN-α and SYY were observed in the animal model. Tumor sizes, lung metastasis, and survival time were assessed. Immunochemistry staining, real-time polymerase chain reaction, and Western blot were used to examine gene expression related to metastasis and angiogenesis in residual cancer after insufficient RFA. Results: For up to 8 weeks of treatment, the combined therapy significantly decreased the residual cancer sizes, minimized the lung metastasis rate, and prolonged the survival time of nude mice, which might be due to suppression of the EMT via β-catenin signal blockade, in addition to attenuating angiogenesis in residual cancer after insufficient RFA. Conclusion: IFN-α combined with SYY significantly weakened the enhanced metastatic potential of residual cancer after insufficient RFA by attenuating EMT, which is mediated through inhibiting activation of β-catenin. In addition, decreasing angiogenesis of residual cancer might also play a certain role.


Oncogene ◽  
2003 ◽  
Vol 22 (54) ◽  
pp. 8662-8670 ◽  
Author(s):  
Mitomu Kioi ◽  
Kazuhiro Yamamoto ◽  
Shouichi Higashi ◽  
Naohiko Koshikawa ◽  
Kiyohide Fujita ◽  
...  

2021 ◽  
Author(s):  
Sangjoon Choi ◽  
Keun-Woo Lee ◽  
Hyun Hee Koh ◽  
Sujin Park ◽  
So-Young Yeo ◽  
...  

Abstract Background: ZMYND8 (zinc finger MYND (Myeloid, Nervy and DEAF-1)-type containing 8) has been known to play an important role in tumor regulation in various types of cancer. However, the results of ZMYND8 expression and their clinical significance in hepatocellular carcinoma (HCC) have not yet been published. In the present study, we investigate the expression of ZMYND8 protein and mRNA in HCC and elucidate its prognostic significance.Methods: ZMYND8 protein and mRNA expression in 283 and 234 HCCs were investigated using immunohistochemistry and quantitative real-time polymerase chain reactions. The relationships between ZMYND8 expression with clinicopathologic features and prognosis of HCC patients were evaluated. Furthermore, we performed the invasion, migration, apoptosis, soft agar formation assay and sphere formation assay in HCC cell lines, and evaluated tumorigenicity in a nude mouse model, after ZMYND8 knockdown. Results: Overexpression of ZMYND8 protein and mRNA was observed in 20.5% and 26.9% of HCC cases, respectively. High ZMYND8 expression showed significant correlations with microvascular invasion, high Edmondson grade, advanced American Joint Committee on Cancer (AJCC), and increased alpha-fetoprotein level. ZMYND8 mRNA overexpression was an independent prognostic factor for predicting early recurrence as well as short recurrence-free survival (RFS). Downregulation of ZMYND8 reduced migration and invasion of HCC cells, and promoted apoptosis of HCC cells in an in vitro model. In a xenograft nude mouse model, knockdown of ZMYND8 significantly reduced tumor growth.Conclusions: ZMYND8 mRNA overexpression could be a prognostic marker of shorter RFS in HCC patients after curative resection. ZMYND8 might play an important role in the proliferation and progression of HCC and could be a promising candidate for targeted therapy.


2001 ◽  
Vol 37 ◽  
pp. S298
Author(s):  
D. Nair ◽  
G. Gallos ◽  
W.L. Yang ◽  
T.S. Ravikumar

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