Su Yang Decoction induces human colon carcinoma cell apoptosis by activating caspases

Ge,Yazhong; Gao,Qing; Yan,Fengjiao; Zhang,Xiaona; Liu,Yurong; Zhou,Yi

doi:10.3892/ol.2018.9625

Su Yang Decoction induces human colon carcinoma cell apoptosis by activating caspases

Authors:
- Yazhong Ge
- Qing Gao
- Fengjiao Yan
- Xiaona Zhang
- Yurong Liu
- Yi Zhou
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Affiliations: Department of Healthy Food Development, Infinitus (China) Company Ltd., Guangzhou, Guangdong 510024, P.R. China, Department of Pharmacology, College of Pharmaceutical Science, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China
Published online on: October 26, 2018 https://doi.org/10.3892/ol.2018.9625
Pages: 422-431

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Abstract

Su Yang Decoction (SYD) is a popular healthcare product comprised of various brassicaceous vegetables known to exhibit anticancer activity. However, the effects of SYD on tumor growth, following its combination with brassicaceous vegetables into a compound formula, require further investigation. In the present study, a quality control of SYD was subjected to high‑performance liquid chromatography for the quantitative and qualitative determination of sulforaphane, the main anticancer component of SYD. SYD inhibited colon cancer cell proliferation in a dose‑ and time‑dependent manner and induced G1 phase arrest in colon cancer HT‑29 cell lines. In addition, SYD triggered caspase‑mediated apoptosis in a dose‑dependent manner and induced the cleavage of poly (ADP‑ribose) polymerase, tumor necrosis factor superfamily member 10, X‑linked inhibitor of apoptosis, and truncated BH3 interacting domain death agonist. Furthermore, the expression of FADD‑like interleukin‑1β‑converting enzyme (FLICE)‑like inhibitory proteins (FLIPs) and long isoform of FLICE‑inhibitory protein was reduced by SYD and the direct targeting of cellular‑FLIP with small interfering RNA inhibited colon cancer cell proliferation and decreased the SYD concentration required for proliferation inhibition. SYD treatment was also associated with the translocation of proapoptotic BCL2 associated X, apoptosis regulator to the mitochondria and the release of cytochrome c from the mitochondria to the cytosol. The aforementioned results indicate that SYD exerts anti‑colorectal cancer effects through an underlying mechanism that may involve caspase activation.

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