Investigation of the possible effect of s-allyl-l-cysteine on apoptosis and autophagy in human leukemia cell line

Abstract

S-Allyl-L-cysteine (SAC) is a biological active organosulfur component of garlic and has various pharmacological effects. SAC has displayed anti-cancer activity but the mechanism is unresolved. This study has focused on investigating the possible apoptotic and autophagic effects of SAC on two human leukemia cell lines: acute promyelocytic leukemia (HL-60) and chronic myeloid leukemia (K562).MATERIAL AND METHODS: Cell cytotoxicity was evaluated via MTT test. Bax, Bcl-2, caspase 3, mTOR, AKT, and PI3K gene expression amounts were identified via Real time quantitative reverse transcription polymerase chain reaction (qRT-PCR). HL-60 and K562 cells were incubated with SAC at three diverse doses (5 mM, 10 mM, and 20 mM) (3,75 mM, 7,5 mM, and 15 mM), respectively.RESULTS: SAC caused a cytotoxic effect on HL-60 and K562 cells with IC50 values of approximately 11.525 mM and 10.025 mM, respectively. In HL-60 cells, an increase in Bax expression levels was detected at doses of 5 mM and 10 mM SAC (p=0.027, p=0.000). Treatment with 10 mM SAC increased the expression level of caspase 3 in HL-60 cells as compared with the control and 5 mM SAC treated cells (p=0.000, p=0.020). In K562 cells, SAC induced a significant decrease in mTOR, AKT, and PI3K expression levels in at all doses (p=0.000, p=0.000, p=0.000).CONCLUSIONS: In conclusion, our data indicates that SAC induces autophagy in K562 cells by downregulating the PI3K/AKT/mTOR signaling pathway. Furthermore, increased Bax and caspase 3 gene expression levels suggest that SAC may be an effective active ingredient with which to induce apoptosis in HL-60 cells.

: S-Allil-L-sistein (SAC), sarımsağın biyolojik olarak aktif bir organosülfür bileşenidir ve çeşitli farmakolojik etkilere sahiptir. SAC anti-kanser aktivite göstermektedir, ancak mekanizması belirlenememiştir. Bu çalışma, SAC'nin iki insan lösemi hücre dizisi üzerindeki olası apoptotik ve otofajik etkilerini araştırmaya odaklanmıştır: akut promiyelositik lösemi (HL-60) ve kronik miyeloid lösemi (K562)