Table 2.

Anti-breast cancer cells activities of artemisinins

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]