Table 2.

Molecular mechanisms of diallyl trisulfide (DATS)-induced apoptosis in cancer cells.

Tumor Type^Ref.	Cell Line	DATS Dose	Observed Changes	Functional Studies and Outcome
Prostate⁵⁴	PC-3, DU145	20-40 μM	↑ROS,↑P-JNK,↑P-Bcl-2, ↓Bcl-2:Bax Interaction	Protection against apoptosis by Bcl-2 and catalase overexpression
Prostate⁵⁵	LNCaP	10-40 μM	↓Bcl-2, ↓Bcl-xL, ↑Bax, ↑Bak, ↑ROS	No effect on apoptosis by Bcl-2 or Bcl-xL overexpression, but protection by Bax/Bak siRNA
Prostate⁵⁷	PC-3, DU145	40-80 μM	↓P-Akt, ↓GSK3-α/β, ↓P-BAD, ↓IGF-1R, ↓PI3K ↓14-3-3β:BAD interaction	Apoptosis inhibition by over- expression of constitutively active Akt and caspase inhibitors
Prostate⁵⁸	LNCaP, DU145	20-40 μM	↓P-JAK2→↓P-STAT3 ↓STAT3 dimer formation	No effect on apoptosis by IL-6 mediated activation of STAT3
Prostate⁵⁹	PC-3, LNCaP	20-40 μM	↓XIAP, ↑survivin, ↑cIAP1	Inhibition of apoptosis by ectopic expression of XIAP but modest effect of survivin or cIAP1 siRNA
Lung⁵⁰	H358, H460	10-40 μM	↓Bcl-2, ↓Bcl-xL, ↑Bax ↑Bak, ↑BID	Apoptosis inhibition by Bax and/or Bak siRNA, but no effect of BID knockdown
Lung⁵¹	A549	12.5-100 μM	↓Bcl-2, ↑P-JNK, ↓P-ERK ↑p53, ↑survivin, ↑ROS	Inhibition of apoptosis by JNK inhibitor and antioxidants
Breast⁶⁹	MDA-MB-231	10-100 μM	↑ROS, ↑P-ASK1, ↑JNK, ↑P-Bim	Protection against cytotoxicity by JNK inhibitor