Table 3.
Anticancer effects of GRg1 on leukemia cancer cell lines
| Aim of study | Results | References | 
|---|---|---|
| ginsenoside effects on induction of apoptosis and inhibition of proliferation in HL-60 cell line | -GRh2 can induce apoptosis and inhibit the cancer cell's proliferation through up-regulation of TNF-α -GRh2 can cause cell cycle arrest in the G1 phase of replication  | 
Huang et al. (2016)21 | 
| Inhibitory effects of GRg1 on the proliferation of leukemia stem cells through SIRT1/TSC2 signaling pathway | -After treatment with GRg1, leukemia cells in the G2/M and S phases of replications were reduced significantly whereas cells in the G0/G1 phase of replication were elevated -Mixed colony-forming unit and beta-galactosidase (senescence markers) were increased significantly -GRg1 can inhibit proliferation and induce senescence markers in leukemia stem cells through activation of the SIRT1 TSC2 signaling pathway  | 
Tang et al. (2020)2 | 
| Induction of senescence in leukemia stem cells by GRg1 through the effect on p16INK4a and hTERT gene expression | -GRg1 can induce Senescence in leukemia stem cells by overexpression of p16INK4a and suppression of hTERT expression | Tang et al. (2021)55 | 
| Effects of GRg1 on K562 leukemia cell line | -After treatment with GRg1, the senescence-related proteins, and beta-galactosidase were increased. Also, GRg1 can inhibit proliferation and colony formation and cause shortened telomere length. It can also alter the morphology of cancer cells by increasing mitochondria size and lysosomes number | Liu et al. (2012)65 | 
| Anti-cancer activity of GRg1 on K562 leukemia cancer cells | -Induction of apoptosis through upregulation of Bax, CPAPR protein, caspase 3, and suppression of Bcl-2, and AG490 -Inhibition of the JAK2/STAT5 pathway and suppression of EpoR expression  | 
Li et al. (2014)56 | 
| Discovering the effects of GRg1 on inducing senescence in K562 leukemia cells by | -Inhibition of K562 cell proliferation and cell cycle arrest in the G2/M phase -Upregulation of senescence-related genes (P16, P21, P53, and Rb)  | 
Cai et al. (2012)54 | 
| Investigation of ginsenoside CK effects against acute myeloid leukemia | -Induction of apoptosis and G1 cell cycle arrest -Upregulation of TET2 gene expression -Downregulation of CSF-1, KIT, BCL2, MYC, and DNMT3A gene expression -In conclusion, CK is a safe and efficient agent against myeloid leukemia cells  | 
Hou et al. (2022)66 | 
| Synergistic activity of ginsenoside CK and cytarabine on acute myeloid leukemia cells | -The cytotoxicity, DNA damage, and apoptosis induced by cytarabine are promoted by ginsenoside CK | Qi et al. (2020)5 | 
| Investigation of CK effects on human leukemia cells | -Induction of apoptosis in leukemia via caspase activation -Inhibition of leukemia cell viability  | 
Cho et al. (2009)67 | 
| Investigation of ginsenoside Rk3 effects on extramedullary infiltration of AML | -Inhibition of extramedullary infiltration of cancer cells -Suppression of invasion, migration, and proliferation of SHI-1 leukemia cells -Increase the expression of mir-3677-5p  | 
Ma et al. (2022)68 | 
| Anticancer effects of ginsenoside Rh1 against acute monocytic leukemia | -Decrease the expression of MCP1 and CCR2 in monocytes -Inhibition of invasion and migration of THP-1 leukemia cell line through suppression of MAPK pathway -Cytotoxicity of GRh2 against leukemia cells wasn't seen in 50µM concentration  | 
Choi et al. (2011)69 |