Effect of down-regulation of phosphoglucose isomerase/autocrine motility factor gene with ginsenoside Rh2 on leukemia KG1α cells in vitro / 中草药

ABSTRACT

Objective: To investigate the down-regulation of phosphoglucose isomerase/autocrine motility factor (PGI/AMF) gene expression by interfering RNA for study on the pharmacological effect of PGI/AMF with ginsenoside Rh2 on leukemia KG1α cells. Methods: The KG1α and the silencing PGI/AMFα KG1α (siPGI-KG1α) cells at logarithmic growth phase were divided into control and drug groups in different dosages. The cells in the control group were normally treated and the cells in the drug groups were incubated with ginsenoside Rh2 in the concentration of 30, 45, 60, 75, and 90 μmol/L in 24, 48, and 72 h respectively. Cell Counting Kit-8 (CCK-8) was used to demonstrate the effect of ginsenside Rh2 on proliferation of KG1α and siPGI-KG1α cells. Trypan blue staining was applied to detecting the effect of human PGI on the proliferation of leukemia KG1α cell. The changes of KG1α by ginsenoside Rh2 on Akt pathway were tested by Antibody Array. The corelation of down-regulating PGI/AMF and Rh2 about mTOR, Raptor, and Rag was detected by Western blotting. Results: Compared with the control group, ginsenoside Rh2 had significant inhibition on the proliferation of KG1α. Down-regulation of PGI/AMF could make KG1α more sensitive to ginsenoside Rh2 and down-regulation of PGI could inhibit the proliferation of KG1α. Antibody Array showed that ginsenoside Rh2 could inhibit the proliferation of KG1α cells through decreasing the expression of P38, mTOR, Akt, AMPKα, PARP, and Bad. Western blotting results indicated that down-regulation of PGI through the synergy of mTOR, Rag, and Raptor with ginsenoside Rh2 could inhibit the proliferation of KG1α cells. Conclusion: Down-regulation of PGI/AMF coordinated with ginsenoside Rh2 could inhibit the proliferation of KG1α cells.