Table 1 Anticancer activity of GS in in vitro experimental model and underlying molecular targets

Pancreatic cancer

Human pancreatic cancer cell lines

↓FXR reduced ↓ NF-κB, ↓Cyclin D1, ↓Bcl-2, ↓XIAP↓MPP9, ↓STAT3, ↓FAK, ↓Src, p-AKT,c-June, ↑Caspase-3,↑Bax

[33, 38, 39]

Head and Neck cancer

Head and neck carcinoma cell line

↓ PI3-kinase/AKT, ↑Bax, ↑Bad

[88]

Esophagael cancer

Esophageal adenocarcinoma cell lines

↓caudal type homeobox 2,↓Cox2,↓NFkB, ↓FXR, ↓ RAR-β2, ↑caspase-8,caspase-9,caspase-3

[47, 48]

Colon cancer

Colon cancer cell line

↓cIAP-1, ↓cIAP-2, ↓Bcl-2, ↓STAT3, ↓VEGF, ↑truncated Bid, ↑Fas, ↑p-JNK, ↑p-c-Jun

[50, 51]

Breast cancer

Breast cancer cell lines

↓cyclin D1, ↓C-myc, ↓survivin, ↓TCF-4, ↓IKK/NF-κB, ↓MAPK/AP-1, ↓MMP-9 ↓

[34, 89]

Prostate cancer

Prostate cancer cell lines

↑caspase-9, ↑caspase-8, ↑caspase-3, ↑Bax

↓Bcl-2 and ↓Bcl-xL

[27]

Hepatocellular carcinoma

Hepatocellular carcinoma cell lines

↓TGF-β1, ↓VEGF,↓ Bcl-2,↑Bax,

↓ NF-κB, ↓STAT3

[83, 85]

Hematological malignancies

Leukemic cell lines

↓Bfl-1/A1, ↓XIAP, ↓cFLIP, ↓Bcl-2, ↓BclXL, ↓survivin

↑caspase 8, ↑bid cleavage, ↑cytochrome c release, ↑caspase 9, ↑ caspase 3, ↑ PARP cleavage.

[25]