The effects of somatostatin on the proliferation of human HepG2 cells and the level of gene p16
Jun-jun Su, Haoliang Zhao
Abstract
Jun-jun Su, Haoliang Zhao
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
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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