Table 2.
Compounds | Effect | Event/mechanism | References |
---|---|---|---|
Artemisinin dimers | Inhibited growth Induced cell death |
Down-regulated the anti-apoptotic protein, survivin, and cyclin D1 Down-regulated the oncogenic protein HER2, HER, declined the wild type epidermal growth factor receptor (EGFR or HER1) |
[77, 78] |
DHA | Induced apoptosis Decreased cell proliferation |
Caused nuclear phospho-TCTP overexpression Increased the Ki-67 expression, synergized with Doxorubicin and Trastuzumab |
[82] |
ART, AS | Arrested cell cycle Decreased cell proliferation |
Increased miR-34a expression, down-regulated the expression of the miR-34a target gene, CDK4, miR-34a required functional p53 | [83] |
DHA | Induced apoptosis Induced G0/G1 arrest |
Increased the expression of caspase-8, cleaved caspase-9, activated Bid, induced the release of cytochrome c from mitochondria into the cytosol, increased the expression of t Bim, decreased the expression of Bcl-2 | [84] |
Tehranolide | Inhibited proliferation Induced G0/G1 arrest Induced apoptosis Increased ROS levels |
Modulated the PI3 K/AKT signaling pathway, increased cytochrome c and Bax, decreased BCL-2, down-regulated ayclin D1, released p27kip1 | [85] |
ART | Inhibited proliferation Induced G1 cell cycle arrest Induced growth arrest of tumorigenic |
Down-regulated the transcript and protein levels of the CDK2 and CDK4 cyclin-dependent kinases, cyclin E, cyclin D1, and the E2F1 transcription factor | [86] |