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

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.

Licochalcone B Extracted from Glycyrrhiza uralensis Fisch Induces Apoptotic Effects in Human Hepatoma Cell HepG2

“…Caspase 3 worked as a key executioner during the latest stages of apoptosis both by extrinsic and intrinsic pathways, which can interact with both Caspase 8 and Caspase 9. 44 The inhibition of Caspase 8 and Caspase 9 proteins in the receptor-mediated pathway and mitochondrial pathway abolished the LCB induced apoptosis significantly. PUMA as an essential intermediate during p53dependent apoptosis can activate the Bax and mitochondrial outer membrane permeabilization.…”

“…In return, activated Caspase 9 can process the downstream caspases, such as Caspase 3. Caspase 3 worked as a key executioner during the latest stages of apoptosis both by extrinsic and intrinsic pathways, which can interact with both Caspase 8 and Caspase 9 . The inhibition of Caspase 8 and Caspase 9 proteins in the receptor-mediated pathway and mitochondrial pathway abolished the LCB induced apoptosis significantly.…”

Enrichment and Evaluation of Antitumor Properties of Total Flavonoids from Juglans mandshurica Maxim

“…After Bak is released in cells subjected to internal stimulation, the mitochondria are destroyed to facilitate the release of cytochrome c, which further contributes to the activation of Caspase9 [50]. It has been reported that activated Caspase 9 is capable of further activating downstream Caspase 3, which interacts with Caspase8 and Caspase9 through the extrinsic and intrinsic pathways and induces apoptosis [51]. All of the above results suggest that the apoptosis of HepG2 cells induced by JMFs exposure may be achieved by affecting the expression regulation of related proteins in the extrinsic and intrinsic pathways (Figure 11).…”