Table 1.
Compounds | Effect | Event/mechanism | References |
---|---|---|---|
Derivatives | Reversed multidrug resistance | Overcoming cross resistance | [31, 61] |
DHA | Induced autophagy Inhibited tumor growth |
Expression of LC3-II, caspase-3 activation, Down-regulation of TfR expression, and cell growth arrested in the G2/M phase | [62] |
DHA | Induced apoptosis | Up-regulated the transcription factor FOXO3a | [63] |
ART-838 | Inhibited cell growth Reduced cell proliferation and clonogenicity Induced apoptosis Increased intracellular levels of ROS |
Increased intracellular ROS levels | [64] |
ART, AS, DHA | Induced apoptosis Increased ROS generation |
Induced cytotoxicity and apoptosis by activated caspase 3/7 Induced ROS generation and lysosomal disruption |
[65] |
DHA | Inhibited tumor growth | Suppressed the expression of Bcr/Abl protein, Reduced the Bcr/Abl tyrosine activity of AKT and ERK1/2, suppressed NF-κB protein expression, Promoted the cytochrome c release and activated caspase3/9 | [66] |
DHA | Induced cell death | Inhibited the Bcr/Abl fusion gene at the mRNA level Inhibited the expression of Bcr/Abl and suppressed the activity of tyrosine kinase, suppressed the downstream signals of Bcr/Abl, reduced the tyrosine kinase activity of AKT and ERK1/2, promoted the cytochrome c release and activated caspase9/3 |
[67] |
AS | Suppressed tumor growth Induced apoptosis |
Suppressed the phosphorylation of p38, ERK, CREB, Chk-2, STAT5, and RSK proteins, Activated caspase-3, inhibited p38, ERK, STAT5, and CREB activation | [68] |