Increased nuclear expression and transactivation of vitamin D receptor by the cardiotonic steroid bufalin in human myeloid leukemia cells

Amano, Yusuke; Cho, Yoshitake; Matsunawa, Manabu; Komiyama, Kanki; Makishima, Makoto

doi:10.1016/j.jsbmb.2009.01.022

Cited by 35 publications

(28 citation statements)

References 53 publications

(69 reference statements)

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“…Resistance to standard chemotherapy is a common clinical problem that requires novel strategies to enhance the antitumorigenic effects of chemotherapeutic agents. Many anticancer agents, including bufalin and Taxol, have been isolated from natural products and are used for the treatment of cancer (2,3). Elemene (1-methyl-1-vinyl-2,4-diisopropenyl-cyclohexane), the active component of the traditional Chinese medicinal herb Rhizoma zedoariae, contains α-, β-and δ-elemene.…”

Section: Introductionmentioning

confidence: 99%

Cbl-regulated Akt and ERK signals are involved in β-elemene-induced cell apoptosis in lung cancer cells

et al. 2011

Mol Med Report

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Abstract. β-elemene is an active component of a natural plantderived antineoplastic agent. Although the anticancer activity of β-elemene has been reported, its antitumor mechanism has not been elucidated. The aim of the present study was to investigate how Cbl-regulated Akt and ERK affect β-elemeneinduced cell apoptosis in lung cancer cells. In the present study, β-elemene induced cell apoptosis in a dose-dependent manner in A549 cells. Moreover, β-elemene decreased bcl-2 expression, increased bax expression and caused the cleavage of PARP. However, β-elemene also induced the phosphorylation of Akt and ERK in a short period of time. The inhibition of Akt and ERK activation rapidly enhanced β-elemene-induced apoptosis, and the up-regulation of c-Cbl and Cbl-b expression was also detected. These results suggest that Cbl-regulated Akt and ERK signals are involved in β-elemene-induced cell apoptosis in lung cancer cells.

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Section: Introductionmentioning

confidence: 99%

Cbl-regulated Akt and ERK signals are involved in β-elemene-induced cell apoptosis in lung cancer cells

et al. 2011

Mol Med Report

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“…1A). Previous reports have demonstrated expression of functional VDR and AHR proteins in U937 cells, THP-1 cells, MCF-7 cells, and HEK293 cells (Hayashi et al, 1995;Campbell et al, 2000;Inaba et al, 2007;Ishizawa et al, 2008;Zhang et al, 2008;Amano et al, 2009). We compared mRNA and protein levels of VDR and AHR in these cell lines.…”

Section: Methodsmentioning

confidence: 96%

Vitamin D Receptor Activation Enhances Benzo[a]pyrene Metabolism via CYP1A1 Expression in Macrophages

et al. 2012

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“…A possible mechanism of the antitumor effect of bufalin may be through the regulation of the MAPK signaling pathway and activation of a variety of transcription factors and protein kinases (14)(15)(16). It has been demonstrated that bufalin induces apoptosis in these cells via the activation of AP-1, the c-Jun N-terminal protein kinase (JNK), as well as by the induction of bcl-2 and the inhibition of protein kinase A.…”

Section: Introductionmentioning

confidence: 99%

Bufalin enhances the antitumor effect of gemcitabine in pancreatic cancer

et al. 2012

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Abstract. Bufalin, an active component of the Chinese medicine chan'su, has been reported to have an inhibitory effect on the growth of various types of cancer cells. In the present study, we investigated whether gemcitabine combined with bufalin enhanced the antitumor efficacy in pancreatic cancer. Three pancreatic cancer cell lines (Bxpc-3, Mia PaCa-2 and Panc-1) were treated with gemcitabine and/or bufalin in vitro. The combination treatment demonstrated greater inhibition of cellular growth and apoptosis. The activity of apoptosis signal-regulating kinase 1 (ASK1)/JNK was upregulated in gemcitabine-induced apoptosis when combined with bufalin. We also observed that tumor growth was significantly inhibited by the combination therapy in a tumor-bearing mouse model, and upregulation of ASK1 activity was validated by immunohistochemical staining. These results suggest that bufalin may be a potential chemotherapeutic agent for pancreatic cancer, which could enhance the antitumor efficacy of gemcitabine when used in combination, possibly through the activation of ASK1/JNK. IntroductionPancreatic cancer is one of the most devastating malignant tumors and the fifth most common cause of cancer-related mortality in developed countries (1). Due to the difficulties of early diagnosis and highly aggressive behavior (2), 85% of patients already have local infiltration or metastasis at the time of diagnosis. Less than 20% of patients have the option of radical tumor resection following the initial diagnosis (3). Thus, the 5-year survival rate of patients with pancreatic cancer is less than 5% (4,5). Apart from surgery, chemotherapy is an essential auxiliary treatment for the management of advanced pancreatic cancer. As the first-line chemotherapy drug for pancreatic cancer, gemcitabine has been widely used in the clinic (6).However, due to a high degree of acquired and inherent resistance to pancreatic cancer chemotherapy (7), up to 20% of pancreatic cancer patients show no obvious effect following treatment with gemcitabine monotherapy (8). Thus, combined therapy with gemcitabine has gained considerable attention in the attempt to improve the outcome of pancreatic cancer (9).Bufalin, an significant active component of the Chinese medicine chan'su (10), has widely demonstrated antitumor effects on human leukemia as well as ovarian, prostate and lung cancer (10-13). A possible mechanism of the antitumor effect of bufalin may be through the regulation of the MAPK signaling pathway and activation of a variety of transcription factors and protein kinases (14-16). It has been demonstrated that bufalin induces apoptosis in these cells via the activation of AP-1, the c-Jun N-terminal protein kinase (JNK), as well as by the induction of bcl-2 and the inhibition of protein kinase A. However, the effect of bufalin on pancreatic cancer cells has not yet been thoroughly evaluated.Apoptosis signal-regulating kinase 1 (ASK1), also known as mitogen-activated protein kinase kinase kinase 5 (MAP3K5), a member of the MAPK family, is a serin...

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Increased nuclear expression and transactivation of vitamin D receptor by the cardiotonic steroid bufalin in human myeloid leukemia cells

Cited by 35 publications

References 53 publications

Cbl-regulated Akt and ERK signals are involved in β-elemene-induced cell apoptosis in lung cancer cells

Cbl-regulated Akt and ERK signals are involved in β-elemene-induced cell apoptosis in lung cancer cells

Vitamin D Receptor Activation Enhances Benzo[a]pyrene Metabolism via CYP1A1 Expression in Macrophages

Bufalin enhances the antitumor effect of gemcitabine in pancreatic cancer

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