Involvement of Caspase-3 in Apoptosis Induced by Viscum album var. coloratum Agglutinin in HL-60 Cells

Lyu, Su Yun; Park, Won Bong; Choi, Kyung Hee; Kim, Won‐Ho

doi:10.1271/bbb.65.534

Cited by 41 publications

(24 citation statements)

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“…coloratum agglutinin (VCA) had cytotoxic effects on cancer cells such as hepatocarcinoma and HL-60 leukemia cells by inducing apoptosis [12,18] . Consistent with this, it was found that VCA selectively killed colon cancer cells (COLO 320HSR) in vitro and in vivo, but not normal human diploid cells (WI-38).…”

Section: Discussionmentioning

confidence: 99%

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Mechanisms involved in Korean mistletoe lectin-induced apoptosis of cancer cells

Khil¹,

Kim²,

Lyu³

et al. 2007

WJG

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AIM:To investigate the anti-cancer mechanisms of Korean mistletoe lectin (Viscum album coloratum agglutinin, VCA) using a human colon cancer cell line (COLO). METHODS:Cytotoxic effects of VCA on COLO cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in vitro and tumor-killing effects in vivo. To study the mechanisms involved, the expression of various pro-caspases, antiapoptotic proteins, and death receptors was determined by western blot. To determine which death receptor is involved in VCA-induced apoptosis of COLO cells, cytotoxicity was examined by MTT assay after treatment with agonists or antagonists of death receptors. RESULTS:VCA killed COLO cells in a time-and dosedependent manner and induced complete regression of tumors in nude mice transplanted with COLO cells. Treatment of COLO cells with VCA activated caspase-2, -3, -8, and -9 and decreased expression of anti-apoptotic molecules including receptor interacting protein, nuclear factor-κB, X-linked inhibitor of apoptosis protein, and Akt/protein kinase B. We then examined the involvement of death receptors in VCA-induced apoptosis. Only tumor necrosis factor receptor 1, among the death receptors examined, was involved in apoptosis of COLO cells, evidenced by inhibition of VCA-induced apoptosis and decreased activation of caspases, particularly caspase-8, by tumor necrosis factor receptor 1 antagonizing antibody. CONCLUSION:VCA-induced apoptotic COLO cell death is due to the activation of caspases and inhibition of antiapoptotic proteins, in part through the tumor necrosis factor receptor 1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

“…VCA showed strong cytotoxic activity against human and murine tumor cells [10] . VCA inhibited telomerase activity, resulting in DNA fragmentation and tumor cell apoptosis [11][12][13] . There are two major pathways for apoptosis: the death receptor-induced pathway and the mitochondriaapoptosome-mediated pathway.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms involved in Korean mistletoe lectin-induced apoptosis of cancer cells

Khil¹,

Kim²,

Lyu³

et al. 2007

WJG

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“…Korean mistletoe (Viscum album L. var. coloratum) is a subspecies of European mistletoe, and has been reported to have cytotoxic and immunological activities similar to European mistletoe [9][10][11][12][13]. A galactose-and N-acetyl-Dgalactosamine-specific lectin (Viscum album L. var.…”

Section: Introductionmentioning

confidence: 99%

Anti-cancer effects of enteric-coated polymers containing mistletoe lectin in murine melanoma cells in vitro and in vivo

et al. 2015

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In this study, we evaluated the effects of Korean mistletoe (Viscum album L. var. coloratum) coated with a biodegradable polymer (Eudragit(®)) wall on the growth of mouse melanoma in vivo. Oral administration of 4% (430 mg/kg/day) enteric-coated mistletoe resulted in a significant reduction in tumor volume on day 14 compared to the negative control group in B16F10 melanoma-inoculated BDF1 mice. When we measured the survival rate, enteric-coated mistletoe-received mice had a higher survival rate after day 12. Also, we investigated the mechanism involving the cancer cell growth inhibition when melanoma cells were treated with Korean mistletoe lectin (Viscum album L. var. coloratum agglutinin, VCA) and its extract in vitro. As a result, a significant G0/G1 arrest was observed in both B16BL6 and B16F10 melanoma cells with VCA or mistletoe extract. In addition, VCA or mistletoe extract induced an increase in both early and late apoptosis in cells. When we studied the molecular mechanism, our results showed that VCA and mistletoe extract can increase activated multiple caspases (caspase-1, 3, 4, 5, 6, 7, 8, and 9), dose-dependently. We also found out that VCA and mistletoe treatment causes a significant decrease in the expression of procaspase-3 and 8.

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“…The N-terminal amino acid and gene sequences of VCA differ from the VAA sequences (Khwaja et al, 1980), but the anticancer effect of VCA is believed to act similarly: the 34-kDa B-chain binds and anchors itself to the tumor cell surface, whereas the 31-kDa A-chain inhibits protein synthesis (Bü ssing et al, 1999;Lyu et al, 2001). However, recent studies report that liquid extracts of Korean mistletoe inhibit tumor metastasis caused by hematogenous and nonhematogenous tumor cells by suppressing tumor growth (Yoon et al, 1995) and inhibiting tumor-induced angiogenesis ).…”

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Critical Role of Reactive Oxygen Species and Mitochondrial Membrane Potential in Korean Mistletoe Lectin-Induced Apoptosis in Human Hepatocarcinoma Cells

Kim

Park²,

Gao³

et al. 2004

Mol Pharmacol

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Viscum album L. coloratum agglutinin (VCA), isolated from Korean mistletoe, is a strong inducer of apoptosis in a variety of tumor cells; however, the underlying molecular mechanisms responsible are not clear. Here, we show that VCA induces apoptotic killing, as demonstrated by DNA fragmentation, Hoechst 33258 staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and flow cytometry analysis in hepatocarcinoma Hep3B cells. VCA treatment results in a significant increase in reactive oxygen species (ROS) and loss of mitochondrial membrane potential (⌬⌿m). Furthermore, treatment with the antioxidant N-acetyl-L-cysteine reduces ROS induction by VCA, preventing apoptosis in Hep3B cells, indicating that oxidative stress is involved in VCA-mediated cell death. Our results also show rapid changes in mitochondrial transition permeability, Bax translocation, cytochrome c release, caspase-3 activity, and poly(ADPribose) polymerase degradation in Hep3B cells occurring in VCAinduced apoptosis. There is much evidence that implicates c-Jun NH 2 -terminal kinase (JNK) activation with apoptosis in a variety of cellular and animal models. In this study, we show that VCA induces JNK phosphorylation, which is abolished with pretreatment with a JNK inhibitor. Moreover, Hep3B cells overexpressing JNK1 or stress-activated protein kinase kinase (SEK1) seem to be more susceptible to cell death from ROS and loss of ⌬⌿m induced by VCA, whereas expression of dominant-negative JNK1 or SEK1 in Hep3B cells do not. These data suggest that JNK phosphorylation may be a major regulator involved in VCAinduced apoptosis. Together, these results suggest that VCA induces apoptosis by inducing ROS production and a loss of ⌬⌿m, in which JNK phosphorylation plays a critical role in these events.

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Involvement of Caspase-3 in Apoptosis Induced by Viscum album var. coloratum Agglutinin in HL-60 Cells

Cited by 41 publications

References 1 publication

Mechanisms involved in Korean mistletoe lectin-induced apoptosis of cancer cells

Mechanisms involved in Korean mistletoe lectin-induced apoptosis of cancer cells

Anti-cancer effects of enteric-coated polymers containing mistletoe lectin in murine melanoma cells in vitro and in vivo

Critical Role of Reactive Oxygen Species and Mitochondrial Membrane Potential in Korean Mistletoe Lectin-Induced Apoptosis in Human Hepatocarcinoma Cells

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