J Zhou1, Z Tang, J Fan. 1. Liver Cancer Institute, Zhongshan Hospital, Shanghai Medical University, Shanghai 200032, China.
Abstract
OBJECTIVE: To investigate the expression of platelet-derived endothelial cell growth factor (PD-ECGF) in liver cancer and explore its related intervention with Capecitabine for the growth and metastasis of liver cancer. METHODS: The protein level of PD-ECGF was determined using immunohistochemical method in 61 HCC samples and the mRNA level was detected using Northern blot analysis. Capecitabine was administered orally in 24 nude mice bearing LCI-D20 tumor. All treatments lasted 3 weeks. The tumor size was calculated by the following formula: V = a x b2 x 0.5. Lung metastasis was evaluated by HE staining in lung samples. RESULTS: The PD-ECGF expression rate in 61 HCC and paratumoral liver tissues was 70.5% and 47.5%, respectively. The rate was higher in HCC tissues with advanced TNM stage than in those with early TNM stage (81.1% vs 54.2%, P < 0.05). The mRNA level of PD-ECGF was related well to its protein expression. The tumor size on day 3 after last treatment measured in the control, and low dose (1.05 mmol.kg-1.day-1), moderate dose (2.10 mmol.kg-1.day-1) and high dose (3.15 mmol.kg-1.day-1) of Capecitabine treatment groups was 447 mm3 +/- 159 mm3, 414 mm3 +/- 97 mm3, 240 mm3 +/- 119 mm3 and 209 mm3 +/- 150 mm3, respectively. High doses of Capecitabine increased the inhibitory effect on the growth and lung metastasis of HCC implant. CONCLUSION: PD-ECGF is highly expressed in HCC and correlates with the TNM staging. Capecitabine may inhibit the growth and metastasis of HCC.
OBJECTIVE: To investigate the expression of platelet-derived endothelial cell growth factor (PD-ECGF) in liver cancer and explore its related intervention with Capecitabine for the growth and metastasis of liver cancer. METHODS: The protein level of PD-ECGF was determined using immunohistochemical method in 61 HCC samples and the mRNA level was detected using Northern blot analysis. Capecitabine was administered orally in 24 nude mice bearing LCI-D20 tumor. All treatments lasted 3 weeks. The tumor size was calculated by the following formula: V = a x b2 x 0.5. Lung metastasis was evaluated by HE staining in lung samples. RESULTS: The PD-ECGF expression rate in 61 HCC and paratumoral liver tissues was 70.5% and 47.5%, respectively. The rate was higher in HCC tissues with advanced TNM stage than in those with early TNM stage (81.1% vs 54.2%, P < 0.05). The mRNA level of PD-ECGF was related well to its protein expression. The tumor size on day 3 after last treatment measured in the control, and low dose (1.05 mmol.kg-1.day-1), moderate dose (2.10 mmol.kg-1.day-1) and high dose (3.15 mmol.kg-1.day-1) of Capecitabine treatment groups was 447 mm3 +/- 159 mm3, 414 mm3 +/- 97 mm3, 240 mm3 +/- 119 mm3 and 209 mm3 +/- 150 mm3, respectively. High doses of Capecitabine increased the inhibitory effect on the growth and lung metastasis of HCC implant. CONCLUSION:PD-ECGF is highly expressed in HCC and correlates with the TNM staging. Capecitabine may inhibit the growth and metastasis of HCC.