Model/cancer cell lines/IC50 Mechanism Pharmacological action References MCF-7μ M G2/M phase arrest, ↓cyclin B, ↓ Cdc2, ↓ Bcl-2 Regulation of the level of proteins which triggered cell cycle blockade at the G2/M phase Liao et al. [103 ] MDA-MB-231μ M ↓ Cdc42↓ Vav2↓ cancer cell migration He et al. [104 ] MCF-7μ M ↓ caspases-3,8, ↓PARP1, ↑Fas-L, ↓Survivin, ↓ERα , ↓cyclin D1, ↓c-Myc, ↓p-Src, ↓ ERK½, ↓p38↓expression of ER-α Chun et al. [105 ] MCF-7μ M ↑ GATA3, ↑ DNMT3A, ↑ ZFPM2, ↑ E-cadherin, ↑ TET2, ↑ TET3, ↓ TET1, ↓ vimentin, ↓ MMP9Diosgenin mediated pathways modulate the GATA3 expression at transcription and translation Aumsuwan et al. [106 ] MDA-MB-231μ g/mL ↓ Bcl-2 ↑ apoptosis via downregulation of proteins related with inhibition Kim et al. [107 ] MCF-7μ M ↓ pAKT (Ser473), ↓ AKT kinase activity, ↓ p-GSK3β , ↓ Raf, ↓ p-MEKs 1/2, ↓ p-MEKs 3/6, ↓ MEK-1, ↓ MEK-4, ↑ pElk-1, ↑ p21, ↓ XIAP, ↓ Bcl-2, ↓ Cdk-2, ↓ Survivin, ↓ cyclin D1, ↓ NF-κ Bp65, ↓ p65, ↑ Iκ B-α , ↓ pElk-1, ↑ Bax, ↓ NF-κ B, ↑ caspase-3 ↑ G1 cell cycle arrest apoptosis in MCF-7 and MDA-231 cells while did not cause in MCF-10A cells Srinivasan et al. [108 ] HuCCT1μ M ↑Bax/Bcl-2, ↑p21, ↑caspase-3, ↑ pARP-1,↓CyclinB1β -PY216β -PS9 G2/M phase arrest Mao et al. [109 ] HT-29μ M ↑ PGE2, ↑ COX-2, ↑ 5-LOX, ↑ LTB4 ↑ apoptosis in both cancer cell lines Lepage et al. [110 ] HCT-116 ↑ ROS, ↑ Ca2+, ↑ NO, ↑ iNOS, ↑ DNA damage, ↑ Gna11, ↑ATP6V0C, ↑Ppp2r5e, ↑COX6C ↑mRNA The compound triggered mitochondrial damage and G2/M cell cycle arrest Chen et al. [111 ] HeLa ↑ caspases-3, 8, 9 Diosgenin and its glycoside derivatives showed strong anticancer activity with low necrotic activity and selective action Hernández-Vázquez et al. [112 ] HeLaμ g/mL ↑ ROS, ↑ Ca2+ , DNA damage, ↑ Bid, Bcl-2, ↓ Bcl-xL, ↑ caspases-3, 9, ↑ Bax, ↑ Bak, ↑ p53 ↑ apoptosis Zhao et al. [113 ] HeLa ↑ apoptosis, ↑ caspase-3 and -9 activity, ↓ Bcl-2 The compound significantly induced apoptosis in a dose and time-dependent manner Cai et al. [114 ] HeLaμ M G2/M phase, ↑ apoptosis, ↑ ROS The compound significantly inhibits cell proliferation, transformed cell morphology, arrests the cell cycle, and regulates apoptosis via death receptor and mitochondrial pathways. Ma et al. [115 ] KYSE510μ M G1/S arrest, ↑ apoptosis, ↑ cleaved caspase-9, ↑ Bax, ↑ Cyt c, ↑ ROS, ↓ Bcl-2 Peroxiredoxins 1 and 6 play an important role in compound induced apoptosis Zhiyu et al. [116 ] NOZμ M ↓ ROS-mediated PI3K/AKT ↑ apoptosis via inhibition of reactive oxygen species-mediated PI3K/AKT signaling Song et al. [117 ] MGC-803μ g/mL ↑ ROS, ↑ Ca2+ , ↑ RBM-3, ↑ GALR-2, ↓ CliC-3, ↓ Bcl-2, ↑ Bax, ↑ caspase-3, 9,↑ MAPKs, ↓ CAP-1, ↓ Tribbles-2 Anticancer effects against human gastric cancer via inducing cell apoptosis, DNA damage, etc. Zhao et al. [118 ] SGC-7901μ g/mL ↑ Fas, ↑ FasL, ↑ TNFR1, ↑ TNF-α , ↓ Bcl-2, ↑ Bax, ↑ Bak, ↓ bid, ↓ Bcl-xL, ↑ p53 mRNA Anticancer activity Hu et al. [119 ] HGC-27μ mol ↓proliferation ↓proliferation of gastric cancer cells Ma et al. [120 ] C6 allograftμ g/mL ↑ROS, ↑Ca2+ , ↑MDA, ↑NO, ↑GSSG, ↓GSH, ↓Bcl-2, Bcl-xL, ↑Bak, ↑Bax, ↑caspase-3, 9 Anticancer activity Lv et al. [121 ] HepG2μ M ↓TAZβ -catenin ↓ cell growth, ↑apoptosis, ↑ apoptosis, ↑G2/M phase arrest Chen et al. [122 ] HepG2μ M G2/M phase arrest, ↑ DDX3, ↓mRNA, ↓ cyclin D1, ↑p21, ↑E-cadherin, ↓ Notch-1, ↓β -catenin ↓ cell growth Yu et al. [123 ] HepG2μ M ↑ caspase-3, 8, 9 ↓ cell growth Kim et al. [124 ] Bel-7402μ mol/L ↑ TP53, ↑ Bax, ↓ Bcl-2 ↓cell growth Zhang et al. [125 ] HepG2μ M ↑ apoptosis, G2/M phase arrest, ↓ cyclin B1, ↑ Bax, ↑ Bcl-2 ↓cell growth Wang et al. [126 ] DU145μ g/mL ↑ LC3-II, ↑ caspase-9, ↓ PI3K, ↓AKT, ↓mTOR, ↑ Beclin-1, ↓ Bcl-2 ↓cell growth Nie et al. [127 ] DU145 ↓vimentin, ↓ Mdm2, ↓ c-Met, ↓ ERK ↑ apoptosis Chang et al. [128 ] PC-3μ M ↓ MMP 2,7,9, ↓mRNA, ↓ EMMPRIN, ↑ TIMP, ↓ AKT, ↓ PI3K, ↓ ERK, ↓c-JNK, ↓NF-κ B, ↓VEGF ↓ cancer cell growth Chen et al. [129 ] PC-3μ M G2/M phase arrest, ↓ NEDD4, ↓ p73, ↑ LATS1, ↓ p-AKT, ↓ TAZ ↓cell growth, ↑apoptosis cell cycle arrest Zhang et al. [130 ] PC3μ M ↑ [Ca2+ ]i, ↑ Mn2+ Significant anticancer activity Sun et al. [131 ]
