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The expression and molecular mechanisms of SH2-B in hepatocarcinoma

Jianjiang Hua, Faqing Tang, Chaojun Duan, Yongmei Yuan, Ya He, Wang Chen

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Abstract

Objective To observe the expression and influence of SH2-B in hepatocarcinoma, and to investigate the molecular mechanisms of canceration in hepatocarcinoma. Methods By using SABC imunohistochemistry, the expressions of SH2-B were detected in 27 cases of hepatitis, 29 cases of hepatocirrhosis and 47 cases of hepatocarcinoma. Hepatocarcinoma cell (HepG) 2 with a low-expressed SH2-B was selected using immunofluorescence assay. There were 3 groups: the transfected group (transfected with pcDNA3.1-SH2-B), the vector group (transfected with pcDNA3.1) and the blank group (without transfection). After gene transfection, SH2-B expression was detected by Western blotting; cell proliferation was measured by MTT assay; cell colony was counted by colony formation test; and cell cycle was analyzed by flowcy tometer. Results The posi-tive rate of SH2-B in hepatocarcinoma (95.7%) was significantly higher than 55.2% in hepatocirrhosis (χ2=18.64, P<0.01) and 25.9% in hepatitis (χ2=40.01, P<0.01). After being transfected with pcDNA 3.1-SH2-B, SH2-B expression dramatically increased in HepG2 cells. After cultured for 48 h, the average optical density value of the transfected group was 1.12±0.19, obviously higher than 0.45±0.11 in the vector group (t=-31.55, P<0.01), which indicated that cells proliferation was significantly enhanced after being transfected with SH2-B. The cell colony numbers of the transfected group was 166±14, significantly higher than 82±8 in the vector group (t=-20.33, P<0.01) and 78±9 in the blank group (t=-19.64, P<0.01), which indicated that the cell colony numbers increased after being transfected with SH2-B. The S stage cells of the transfected group was (45.7±5.8)%, significantly higher than (19.4±4.7)% in the vector group (t=-20.33, P<0.01) and (20.5±5.1)% in the blank group (t=-34.69, P<0.01), which indicated that SH2-B could enhance promote cell cycle of HepG2 cells. Conclusion The expression of SH2-B in hepatocarcinoma is high, and it may be involved in the canceration of hepatocarcinoma though promoting cell cycle, cell proliferation and cell transformation. Key words: Liver neoplasms; SH2-B; Molecular mechanisms

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Objective To observe the expression and influence of SH2-B in hepatocarcinoma, and to investigate the molecular mechanisms of canceration in hepatocarcinoma. Methods By using SABC imunohistochemistry, the expressions of SH2-B were detected in 27 cases of hepatitis, 29 cases of hepatocirrhosis and 47 cases of hepatocarcinoma. Hepatocarcinoma cell (HepG) 2 with a low-expressed SH2-B was selected using immunofluorescence assay. There were 3 groups: the transfected group (transfected with pcDNA3.1-SH2-B), the vector group (transfected with pcDNA3.1) and the blank group (without transfection). After gene transfection, SH2-B expression was detected by Western blotting; cell proliferation was measured by MTT assay; cell colony was counted by colony formation test; and cell cycle was analyzed by flowcy tometer. Results The posi-tive rate of SH2-B in hepatocarcinoma (95.7%) was significantly higher than 55.2% in hepatocirrhosis (χ2=18.64, P<0.01) and 25.9% in hepatitis (χ2=40.01, P<0.01). After being transfected with pcDNA 3.1-SH2-B, SH2-B expression dramatically increased in HepG2 cells. After cultured for 48 h, the average optical density value of the transfected group was 1.12±0.19, obviously higher than 0.45±0.11 in the vector group (t=-31.55, P<0.01), which indicated that cells proliferation was significantly enhanced after being transfected with SH2-B. The cell colony numbers of the transfected group was 166±14, significantly higher than 82±8 in the vector group (t=-20.33, P<0.01) and 78±9 in the blank group (t=-19.64, P<0.01), which indicated that the cell colony numbers increased after being transfected with SH2-B. The S stage cells of the transfected group was (45.7±5.8)%, significantly higher than (19.4±4.7)% in the vector group (t=-20.33, P<0.01) and (20.5±5.1)% in the blank group (t=-34.69, P<0.01), which indicated that SH2-B could enhance promote cell cycle of HepG2 cells. Conclusion The expression of SH2-B in hepatocarcinoma is high, and it may be involved in the canceration of hepatocarcinoma though promoting cell cycle, cell proliferation and cell transformation. Key words: Liver neoplasms; SH2-B; Molecular mechanisms

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Available abstract

Objective To observe the expression and influence of SH2-B in hepatocarcinoma, and to investigate the molecular mechanisms of canceration in hepatocarcinoma. Methods By using SABC imunohistochemistry, the expressions of SH2-B were detected in 27 cases of hepatitis, 29 cases of hepatocirrhosis and 47 cases of hepatocarcinoma. Hepatocarcinoma cell (HepG) 2 with a low-expressed SH2-B was selected using immunofluorescence assay. There were 3 groups: the transfected group (transfected with pcDNA3.1-SH2-B), the vector group (transfected with pcDNA3.1) and the blank group (without transfection). After gene transfection, SH2-B expression was detected by Western blotting; cell proliferation was measured by MTT assay; cell colony was counted by colony formation test; and cell cycle was analyzed by flowcy tometer. Results The posi-tive rate of SH2-B in hepatocarcinoma (95.7%) was significantly higher than 55.2% in hepatocirrhosis (χ2=18.64, P<0.01) and 25.9% in hepatitis (χ2=40.01, P<0.01). After being transfected with pcDNA 3.1-SH2-B, SH2-B expression dramatically increased in HepG2 cells. After cultured for 48 h, the average optical density value of the transfected group was 1.12±0.19, obviously higher than 0.45±0.11 in the vector group (t=-31.55, P<0.01), which indicated that cells proliferation was significantly enhanced after being transfected with SH2-B. The cell colony numbers of the transfected group was 166±14, significantly higher than 82±8 in the vector group (t=-20.33, P<0.01) and 78±9 in the blank group (t=-19.64, P<0.01), which indicated that the cell colony numbers increased after being transfected with SH2-B. The S stage cells of the transfected group was (45.7±5.8)%, significantly higher than (19.4±4.7)% in the vector group (t=-20.33, P<0.01) and (20.5±5.1)% in the blank group (t=-34.69, P<0.01), which indicated that SH2-B could enhance promote cell cycle of HepG2 cells. Conclusion The expression of SH2-B in hepatocarcinoma is high, and it may be involved in the canceration of hepatocarcinoma though promoting cell cycle, cell proliferation and cell transformation. Key words: Liver neoplasms; SH2-B; Molecular mechanisms

Key concepts: Transfection, Molecular biology, Immunofluorescence, Blot, Cell growth, Hepatitis B virus, Group A, Cell cycle

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