2010肿瘤研究与临床Requires access

The effects of somatostatin on the proliferation of human HepG2 cells and the level of gene p16

Jun-jun Su, Haoliang Zhao

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Abstract

Objective To study the effect of somatostatin on the Proliferation in Human HepG2 Cells and the Level of Gene p16. Methods The cell line HepG2 were divided into 3 groups: control groupA, low concentration group B and high concentration group C. The flow cytometry (FCM) was used to detect phase distribution of the cycles and detect the expression of p16 gene by using RT-PCR. Results Human HepG2 cells affected 24 hours later by different density SST, using FCM, we discovered that the G1 cell cycles of each A group, B group, C group occupied the proportion respectively is (51.41±3.27)%, (65.43±3.41)%, (69.02±3.75)%, that the S cell cycles is (36.86±2.31)%, (20.34±2.52)%, (18.50±3.09)%, that the G2 cell cycles is (11.46±1.96)%, (14.23±3.83)%, (12.48±3.18)%. Compare to the control groupA, the G1 cell cycles of groupB and group C were increased obviously. But the S cell cycles relatively reduced. The levels of p16 gene were expressed in each group detected by RT-PCR, but B group and C group expressed obviously. Conclusion The inhibited mechanism of somatostatin for HepG2 was expressed probably by improving levels of p16. Key words: Somatostatin;  Genes, p16;  Cell cycle;  Liver neoplasms

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Objective To study the effect of somatostatin on the Proliferation in Human HepG2 Cells and the Level of Gene p16. Methods The cell line HepG2 were divided into 3 groups: control groupA, low concentration group B and high concentration group C. The flow cytometry (FCM) was used to detect phase distribution of the cycles and detect the expression of p16 gene by using RT-PCR. Results Human HepG2 cells affected 24 hours later by different density SST, using FCM, we discovered that the G1 cell cycles of each A group, B group, C group occupied the proportion respectively is (51.41±3.27)%, (65.43±3.41)%, (69.02±3.75)%, that the S cell cycles is (36.86±2.31)%, (20.34±2.52)%, (18.50±3.09)%, that the G2 cell cycles is (11.46±1.96)%, (14.23±3.83)%, (12.48±3.18)%. Compare to the control groupA, the G1 cell cycles of groupB and group C were increased obviously. But the S cell cycles relatively reduced. The levels of p16 gene were expressed in each group detected by RT-PCR, but B group and C group expressed obviously. Conclusion The inhibited mechanism of somatostatin for HepG2 was expressed probably by improving levels of p16. Key words: Somatostatin;  Genes, p16;  Cell cycle;  Liver neoplasms

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Available abstract

Objective To study the effect of somatostatin on the Proliferation in Human HepG2 Cells and the Level of Gene p16. Methods The cell line HepG2 were divided into 3 groups: control groupA, low concentration group B and high concentration group C. The flow cytometry (FCM) was used to detect phase distribution of the cycles and detect the expression of p16 gene by using RT-PCR. Results Human HepG2 cells affected 24 hours later by different density SST, using FCM, we discovered that the G1 cell cycles of each A group, B group, C group occupied the proportion respectively is (51.41±3.27)%, (65.43±3.41)%, (69.02±3.75)%, that the S cell cycles is (36.86±2.31)%, (20.34±2.52)%, (18.50±3.09)%, that the G2 cell cycles is (11.46±1.96)%, (14.23±3.83)%, (12.48±3.18)%. Compare to the control groupA, the G1 cell cycles of groupB and group C were increased obviously. But the S cell cycles relatively reduced. The levels of p16 gene were expressed in each group detected by RT-PCR, but B group and C group expressed obviously. Conclusion The inhibited mechanism of somatostatin for HepG2 was expressed probably by improving levels of p16. Key words: Somatostatin;  Genes, p16;  Cell cycle;  Liver neoplasms

Key concepts: Somatostatin, Flow cytometry, Cell cycle, Cell growth, Gene, Molecular biology, Somatostatin receptor 2, Cell

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