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Sorafenib suppresses the epithelial-mesenchymal transition of hepatocellular carcinoma cells after insufficient radiofrequency ablation.

Dong S, Kong J, Kong F, Kong J, Gao J, Ji L, Pan B, Chen L, Zheng L, Sun W - BMC Cancer (2015)

Bottom Line: An ectopic nude mice model was used to evaluate the effect of sorafenib on the growth of HepG2 cells in vivo after insufficient RFA.Higher expression of PCNA, Ki67, N-cadherin, MMP-2 and MMP-9, was also observed in HepG2-H tumors.Sorafenib blocked the enhanced growth of HepG2 cells in vivo after insufficient RFA.

View Article: PubMed Central - PubMed

Affiliation: Department of Hepatobiliary Surgery, Beijing Chao-yang Hospital, Capital Medical University, Beijing, 100043, China. shuying19870219@163.com.

ABSTRACT

Background: Epithelial-mesenchymal transition (EMT) played an important role in the progression of hepatocellular carcinoma (HCC) after insufficient radiofrequency ablation (RFA). However, whether sorafenib could be used to suppress the EMT of HCC after insufficient RFA and further prevent the progression of residual HCC remains poorly unknown.

Methods: Insufficient RFA was simulated using a water bath (47 °C 5, 10, 15, 20 and 25 min gradually). MTT assay and transwell assay were used to evaluate the effects of sorafenib on viability, migration and invasion of HepG2 and SMMC7721 cells after insufficient RFA in vitro. After insufficient RFA, the molecular changes in HCC cells with the treatment of sorafeinb were evaluated using western blot and ELISAs. An ectopic nude mice model was used to evaluate the effect of sorafenib on the growth of HepG2 cells in vivo after insufficient RFA.

Results: HepG2 and SMMC7721 cells after insufficient RFA (named as HepG2-H and SMMC7721-H) exhibited enhanced viability, migration and invasion in vitro. Sorafenib inhibited the enhanced viability, migration and invasion of HepG2 and SMMC7721 cells after insufficient RFA. Molecular changes of EMT were observed in HepG2-H and SMMC7721-H cells. Sorafenib inhibited the EMT of HepG2-H and SMMC7721-H cells. HepG2-H cells also exhibited larger tumor size in vivo. Higher expression of PCNA, Ki67, N-cadherin, MMP-2 and MMP-9, was also observed in HepG2-H tumors. Sorafenib blocked the enhanced growth of HepG2 cells in vivo after insufficient RFA.

Conclusions: Sorafenib inhibited the EMT of HCC cells after insufficient RFA, and may be used to prevent the progression of HCC after RFA.

No MeSH data available.


Related in: MedlinePlus

Insufficient RFA enhanced the growth of HCC cells in vivo, and sorafenib blocked the process. HepG2 and HepG2-H cells were injected subcutaneously into the upper right flank region of nude mice, treated with or without sorafenib, and tumor volume was measured. (a) Tumor volume was measured with a caliper rule every other day. Data were presented as the mean tumor volumes of mice. (b) Tumor size of the 29th day was displayed. (c) Tumor sections were stained for PCNA, Ki67, MMP-2, MMP-9, E-cadherin and N-cadherin. Representive images of the immunohistochemistry assay were shown (200×)
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Fig5: Insufficient RFA enhanced the growth of HCC cells in vivo, and sorafenib blocked the process. HepG2 and HepG2-H cells were injected subcutaneously into the upper right flank region of nude mice, treated with or without sorafenib, and tumor volume was measured. (a) Tumor volume was measured with a caliper rule every other day. Data were presented as the mean tumor volumes of mice. (b) Tumor size of the 29th day was displayed. (c) Tumor sections were stained for PCNA, Ki67, MMP-2, MMP-9, E-cadherin and N-cadherin. Representive images of the immunohistochemistry assay were shown (200×)

Mentions: HepG2-H cells showed increased tumor volume compared with HepG2 cells (Fig. 5a and b). Sorafenib suppressed the growth of HepG2 and HepG2-H cells (Fig. 5a and b). Sorafenib diminished the difference of tumor growth between HepG2 and HepG2-H cells (Fig. 5a and b). Significant increases of cell proliferation were observed in HepG2-H cells, and sorafenib inhibited the process (Fig. 5c). In addition, HepG2-H tumors showed decreased expression of E-cadherin and increased expression of N-cadherin, MMP-2 and MMP-9 compared with HepG2 tumors (Fig. 5c). And sorafenib increased the expression of E-cadherin, and decreased the expression of N-cadherin, MMP-2 and MMP-9 in HepG2 and HepG2-H tumors (Fig. 5c). However, there were no apparent changes in liver, heart, kidney, lung and body weight in the mice (Additional file 2: Figure S4).Fig. 5


Sorafenib suppresses the epithelial-mesenchymal transition of hepatocellular carcinoma cells after insufficient radiofrequency ablation.

Dong S, Kong J, Kong F, Kong J, Gao J, Ji L, Pan B, Chen L, Zheng L, Sun W - BMC Cancer (2015)

Insufficient RFA enhanced the growth of HCC cells in vivo, and sorafenib blocked the process. HepG2 and HepG2-H cells were injected subcutaneously into the upper right flank region of nude mice, treated with or without sorafenib, and tumor volume was measured. (a) Tumor volume was measured with a caliper rule every other day. Data were presented as the mean tumor volumes of mice. (b) Tumor size of the 29th day was displayed. (c) Tumor sections were stained for PCNA, Ki67, MMP-2, MMP-9, E-cadherin and N-cadherin. Representive images of the immunohistochemistry assay were shown (200×)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4663721&req=5

Fig5: Insufficient RFA enhanced the growth of HCC cells in vivo, and sorafenib blocked the process. HepG2 and HepG2-H cells were injected subcutaneously into the upper right flank region of nude mice, treated with or without sorafenib, and tumor volume was measured. (a) Tumor volume was measured with a caliper rule every other day. Data were presented as the mean tumor volumes of mice. (b) Tumor size of the 29th day was displayed. (c) Tumor sections were stained for PCNA, Ki67, MMP-2, MMP-9, E-cadherin and N-cadherin. Representive images of the immunohistochemistry assay were shown (200×)
Mentions: HepG2-H cells showed increased tumor volume compared with HepG2 cells (Fig. 5a and b). Sorafenib suppressed the growth of HepG2 and HepG2-H cells (Fig. 5a and b). Sorafenib diminished the difference of tumor growth between HepG2 and HepG2-H cells (Fig. 5a and b). Significant increases of cell proliferation were observed in HepG2-H cells, and sorafenib inhibited the process (Fig. 5c). In addition, HepG2-H tumors showed decreased expression of E-cadherin and increased expression of N-cadherin, MMP-2 and MMP-9 compared with HepG2 tumors (Fig. 5c). And sorafenib increased the expression of E-cadherin, and decreased the expression of N-cadherin, MMP-2 and MMP-9 in HepG2 and HepG2-H tumors (Fig. 5c). However, there were no apparent changes in liver, heart, kidney, lung and body weight in the mice (Additional file 2: Figure S4).Fig. 5

Bottom Line: An ectopic nude mice model was used to evaluate the effect of sorafenib on the growth of HepG2 cells in vivo after insufficient RFA.Higher expression of PCNA, Ki67, N-cadherin, MMP-2 and MMP-9, was also observed in HepG2-H tumors.Sorafenib blocked the enhanced growth of HepG2 cells in vivo after insufficient RFA.

View Article: PubMed Central - PubMed

Affiliation: Department of Hepatobiliary Surgery, Beijing Chao-yang Hospital, Capital Medical University, Beijing, 100043, China. shuying19870219@163.com.

ABSTRACT

Background: Epithelial-mesenchymal transition (EMT) played an important role in the progression of hepatocellular carcinoma (HCC) after insufficient radiofrequency ablation (RFA). However, whether sorafenib could be used to suppress the EMT of HCC after insufficient RFA and further prevent the progression of residual HCC remains poorly unknown.

Methods: Insufficient RFA was simulated using a water bath (47 °C 5, 10, 15, 20 and 25 min gradually). MTT assay and transwell assay were used to evaluate the effects of sorafenib on viability, migration and invasion of HepG2 and SMMC7721 cells after insufficient RFA in vitro. After insufficient RFA, the molecular changes in HCC cells with the treatment of sorafeinb were evaluated using western blot and ELISAs. An ectopic nude mice model was used to evaluate the effect of sorafenib on the growth of HepG2 cells in vivo after insufficient RFA.

Results: HepG2 and SMMC7721 cells after insufficient RFA (named as HepG2-H and SMMC7721-H) exhibited enhanced viability, migration and invasion in vitro. Sorafenib inhibited the enhanced viability, migration and invasion of HepG2 and SMMC7721 cells after insufficient RFA. Molecular changes of EMT were observed in HepG2-H and SMMC7721-H cells. Sorafenib inhibited the EMT of HepG2-H and SMMC7721-H cells. HepG2-H cells also exhibited larger tumor size in vivo. Higher expression of PCNA, Ki67, N-cadherin, MMP-2 and MMP-9, was also observed in HepG2-H tumors. Sorafenib blocked the enhanced growth of HepG2 cells in vivo after insufficient RFA.

Conclusions: Sorafenib inhibited the EMT of HCC cells after insufficient RFA, and may be used to prevent the progression of HCC after RFA.

No MeSH data available.


Related in: MedlinePlus