Type of cancer | Samples | Dose range | Cell line | Target | Pathway | Function | Refs. |
---|---|---|---|---|---|---|---|
Leukemia | In vitro | 10Â mM | K562/ADR, K562 | P-gp, Caspase-3/8, ERK1/2, JNK | PI3K/AKT/mTOR | RVT via suppressing the PI3K/AKT/mTOR pathway could increase the anti-proliferative activity of bestatin | [59] |
Leukemia | In vitro | 0–20 μM | PBMCs, HL-60, NB-4 | – | PTEN/PI3K/AKT | RVT via regulating the PTEN/PI3K/AKT pathway could affect apoptosis and proliferation of leukemia cells | [60] |
Acute Myeloid Leukemia (AML) | In vitro | 25–200 lmol/L | HL-60, HL-60/ADR | MRP1 | PI3K/AKT/Nrf2 | RVT via the PI3K/AKT/Nrf2 Pathway could reverse the drug resistance of AML HL-60/ADR cells | [61] |
Chronic Myeloid Leukemia (CML) | In vitro | 60 μM | K562 | p70S6K, 4EBP1, Cyclin-D1, Caspase-3, | PI3K/AKT/mTOR | RVT via downregulating the PI3K/AKT/mTOR pathway could play a role in the apoptosis of K562 cells | [62] |