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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

Sorafenib inhibited the enhanced viability of HCC cells after insufficient RFA. HepG2 cells were treated with insufficient RFA (47 °C 5 min, 10 min, 15 min, 20 min and 25 min) gradually. Residual HepG2 (named as HepG2-H) cells surviving from the treatment of 47 °C for 25 min were collected and used for the next experiments. (a) The effect of sorafenib on viability rate of HepG2 and HepG2-H cells was evaluated by MTT assay. Error bars represent the SEM of data obtained in five independent experiments. (b and c) Colony formation abilities of HepG2 and HepG2-H cells after the treatment of sorafenib were assessed. Representive images of the colonies were shown (12.5×) Error bars represent the SEM of data obtained in three independent experiments. P value <0.05 was considered statistically significant; **p < 0.01, ***p < 0.001
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Fig1: Sorafenib inhibited the enhanced viability of HCC cells after insufficient RFA. HepG2 cells were treated with insufficient RFA (47 °C 5 min, 10 min, 15 min, 20 min and 25 min) gradually. Residual HepG2 (named as HepG2-H) cells surviving from the treatment of 47 °C for 25 min were collected and used for the next experiments. (a) The effect of sorafenib on viability rate of HepG2 and HepG2-H cells was evaluated by MTT assay. Error bars represent the SEM of data obtained in five independent experiments. (b and c) Colony formation abilities of HepG2 and HepG2-H cells after the treatment of sorafenib were assessed. Representive images of the colonies were shown (12.5×) Error bars represent the SEM of data obtained in three independent experiments. P value <0.05 was considered statistically significant; **p < 0.01, ***p < 0.001

Mentions: First of all, HepG2 or SMMC7721 cells were treated with heat treatment for 5, 10, 15, 20 and 25 min gradually as described above. Cells surviving from the treatment of 47 °C for 25 min were designated as HepG2-H and SMMC7721-H cells when we could see the morphological changes. To evaluate the effects of sorafenib on HCC cells, all cells were treated with sorafenib for 24, 48 or 72 h at different concentrations. HepG2-H cells exhibited higher viability rate compared with HepG2 cells at 48 and 72 h (Fig. 1a). Sorafenib inhibited the viability rate of HepG2 and HepG2-H cells in a time- and dose- dependent manner (Fig. 1a). After the treatment of sorafenib (5 and 10 μM) for 24 and 48 h and sorafenib (2, 5 and 10 μM) for 72 h, the distinction of viability rate between HepG2 and HepG2-H cells faded (Fig. 1a). To determine the long term growth ability, sorafenib was allowed to treated HCC cells for 2 weeks. HepG2-H cells had a higher number of colonies in comparison with HepG2 cells (Fig. 1b and c). Sorafenib also suppressed the colony formation of HepG2 and HepG2-H cells in a dose-dependent manner. Similar results were also found in SMMC7721 and SMMC7721-H cells (Additional file 2: Figure S1).Fig. 1


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)

Sorafenib inhibited the enhanced viability of HCC cells after insufficient RFA. HepG2 cells were treated with insufficient RFA (47 °C 5 min, 10 min, 15 min, 20 min and 25 min) gradually. Residual HepG2 (named as HepG2-H) cells surviving from the treatment of 47 °C for 25 min were collected and used for the next experiments. (a) The effect of sorafenib on viability rate of HepG2 and HepG2-H cells was evaluated by MTT assay. Error bars represent the SEM of data obtained in five independent experiments. (b and c) Colony formation abilities of HepG2 and HepG2-H cells after the treatment of sorafenib were assessed. Representive images of the colonies were shown (12.5×) Error bars represent the SEM of data obtained in three independent experiments. P value <0.05 was considered statistically significant; **p < 0.01, ***p < 0.001
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig1: Sorafenib inhibited the enhanced viability of HCC cells after insufficient RFA. HepG2 cells were treated with insufficient RFA (47 °C 5 min, 10 min, 15 min, 20 min and 25 min) gradually. Residual HepG2 (named as HepG2-H) cells surviving from the treatment of 47 °C for 25 min were collected and used for the next experiments. (a) The effect of sorafenib on viability rate of HepG2 and HepG2-H cells was evaluated by MTT assay. Error bars represent the SEM of data obtained in five independent experiments. (b and c) Colony formation abilities of HepG2 and HepG2-H cells after the treatment of sorafenib were assessed. Representive images of the colonies were shown (12.5×) Error bars represent the SEM of data obtained in three independent experiments. P value <0.05 was considered statistically significant; **p < 0.01, ***p < 0.001
Mentions: First of all, HepG2 or SMMC7721 cells were treated with heat treatment for 5, 10, 15, 20 and 25 min gradually as described above. Cells surviving from the treatment of 47 °C for 25 min were designated as HepG2-H and SMMC7721-H cells when we could see the morphological changes. To evaluate the effects of sorafenib on HCC cells, all cells were treated with sorafenib for 24, 48 or 72 h at different concentrations. HepG2-H cells exhibited higher viability rate compared with HepG2 cells at 48 and 72 h (Fig. 1a). Sorafenib inhibited the viability rate of HepG2 and HepG2-H cells in a time- and dose- dependent manner (Fig. 1a). After the treatment of sorafenib (5 and 10 μM) for 24 and 48 h and sorafenib (2, 5 and 10 μM) for 72 h, the distinction of viability rate between HepG2 and HepG2-H cells faded (Fig. 1a). To determine the long term growth ability, sorafenib was allowed to treated HCC cells for 2 weeks. HepG2-H cells had a higher number of colonies in comparison with HepG2 cells (Fig. 1b and c). Sorafenib also suppressed the colony formation of HepG2 and HepG2-H cells in a dose-dependent manner. Similar results were also found in SMMC7721 and SMMC7721-H cells (Additional file 2: Figure S1).Fig. 1

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