Effect of Angelica keiskei Extract on Apoptosis of MDA-MB-231 Human Breast Cancer Cells

Abstract

We investigated the effect of Angelica keiskei ethanol (AKE) extract on cell death in MDA-MB-231 human breast cancer cells. MDA-MB-231 cells were cultured in the presence 125, 150 and 175 μg/mL concentrations of AKE for 24 hours. MTT assays demonstrated that mitochondrial dehydrogenase activities decreased in a dose-dependent manner in MDA-MB-231 cells (p<0.05). In contrast, the proportion of dual staining with Hoechst 33342/ethidium bromide(EtBr) for cell death increased in a dose-dependent manner in MDA-MB-231 cells (p< 0.05). In particular, the levels of cell death caused by apoptotic program showed marked increases in the 150 and 175 μg/mL AKE groups, as revealed by flow cytometry. An apoptotic suppressor gene, Bcl-2, significantly decreased at the transcript level (p<0.05). The expression levels of proapoptotic genes, both Bax and caspase 3 significantly increased (p<0.05). Furthermore, the ratio of Bcl-2/Bax mRNA which is considered to be an important indicator of apoptosis, significantly decreased in a dose-dependent manner (p<0.05). These results taken together indicate that, the AKE extract used in this study induces cell death in MDA-MB-231 human breast cancer cells.

A comprehensive review of antitumor properties of Angelica species and their antitumor‐responsible constituents and the underlying molecular mechanisms involved in tumor inhibition

“…A . keiskei ethanol (AKE) extract markedly induced cell death in human breast cancer cells and significantly decreased the Bcl‐2 (apoptotic suppressor gene) level, increased the expression of Bax and caspase 3 (proapoptotic genes) and the ratio of Bcl‐2/Bax mRNA was decreased, leading to cell death of breast cancer cells (Jeong & Kang, 2011). A number of valuable research studies have been conducted to reveal the anticancer effects of bergapten (5‐methoxypsoralen), from other medicinal plant sources, including some species of Angelica genus, as well as from synthetic sources on various cancer types (Liang et al, 2021; Quetglas‐Llabrés et al, 2022).…”

“…To date, various species of the Angelica genus have been reported to possess antitumor properties including, Angelica acutiloba (Roh et al, 2012), Angelica atropurpurea (Kontogiorgis et al, 2012), Angelica archangelica , Angelica dahuria (Dong et al, 2021; Kim et al, 2007), Angelica edulis (Wang, Sun, et al, 2014; Wang, Xiao, et al, 2014), Angelica keiskei ( Jeong et al, 2011), Angelica glauca (Kumar et al, 2022), Angelica japonica (Kimura et al, 2008), Angelica amurensis (Jung et al, 2018), Angelica polymorpha (Rahman et al, 2016), Angelica sylvestris (Raal et al, 2022), Angelica shikokiana (Mira et al, 2017), Angelica sinensis , and Angelica gigas (Kim et al, 2022) (Figure 1). Through extensive literature study about Angelica species, specifically focusing on A .…”

Angelica keiskei, an emerging medicinal herb with various bioactive constituents and biological activities

“…. In these cancer cell lines studies, increasing expression level of the proapoptotic gene, Caspase-3, and apoptotic inducer gene, B cell lymphoma 2 (Bcl-2), and decreasing expression level of the apoptotic suppressor gene, Bcl-2 associated x (Bax), were presented as the mechanism of action of anti-cancer effects of A. keiskei (Jeong and Kang 2011). The methanol extract showed an anti-mutagenic activity against aflatoxin B1 (AFB1), N-methyl-N 0 -nitro-N-nitrosoguanidine, Kozawa et al (1977) RT Anti-ulcer activity: gastric H ?…”

Natural 2′,4-Dihydroxy-4′,6′-dimethoxy Chalcone Isolated from Chromolaena tacotana Inhibits Breast Cancer Cell Growth through Autophagy and Mitochondrial Apoptosis

“…Isobavachalcone, sourced from Psoralea corylifolia L, enhances sensitivity to E2-induced paclitaxel resistance by down-regulating CD44 expression in ER-positive breast cancer cells [ 12 ]. Additionally, a prenylated chalcone named Xanthoangelol B, isolated from Ashitaba (Angelica keiskei Koidzumi, Apiaceae), induces apoptotic cell death through the activation of caspase-3, via a mechanism that does not involve the Bax/Bcl-2 signal transduction pathway [ 13 ].…”