. 2018 Apr 9;8(4):303–319. doi: 10.1007/s13659-018-0162-1

Table 7.

Anti-gastric cancer cells activities of artemisinins

Compounds	Effect	Event/mechanism	References
ART	Inhibited proliferation	Up-regulated p53, induce p27^kip1 andp21^kip1	[20]
AS	Inhibited proliferation Induced apoptosis	Reduced COX-2 expression, increased the expression of Bax and suppressed the expression of Bcl-2, activated caspase-3 and caspase-9, induced loss of mitochondrial membrane potential	[38]
AS	Inhibited cell growth	Induced calcium overload, down-regulated VEGF expression, up-regulated calpain-2 expression, produced a dose-dependent tumor regression	[38]
DHA	Inhibited proliferation Suppressed colony forming abilities Induced cellular senescence Induced cell cycle arrest Hindered the migration and invasion Induced apoptosis	Suppressed the expressions of PCNA, cyclin E, and cyclin D1, and up-regulated p21 and p27, down-regulated MMP-9 and MMP-2, suppressed Bcl-2, activated caspase-9 and PARP, increased miR-15b and miR-16 expression	[110]
DHA	Induced apoptosis	Up-regulated Bax, cleaved caspase-3 and -9 expressions, degraded form of PARP, downregulated the Bcl-2 expression and Bcl-2/Bax ratio, increased the phosphorylation of ERK1/2, JNK1/2 and p38 MAPK	[111]
ATM	Cytotoxic genotoxic effects	Induced both apoptosis and necrosis	[112]