Moscatilin Induces Apoptosis and Mitotic Catastrophe in Human Esophageal Cancer Cells

Chen, Chien-An; Chen, Chien-Chih; Shen, Chien‐Chang; Chang, Hen‐Hong; Chen, Yu-Jen

doi:10.1089/jmf.2012.2617

Cited by 30 publications

(27 citation statements)

References 30 publications

(33 reference statements)

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“…Furthermore, moscatilin was revealed to strongly suppress pancreatic tumor growth and development, without any apparent toxicity, in vivo . In previous studies, moscatilin has been demonstrated to possess proapoptotic effects in esophageal cancer, antimetastatic effects in lung and breast cancer, and anti-angiogenic activity against malignant tumors (16–19). These previous data indicated that moscatilin is worthy of being developed into a therapeutic agent for the prevention and treatment of pancreatic cancer.…”

Section: Discussionmentioning

confidence: 99%

“…denneanum , was revealed to exert proapoptotic effects in pancreatic cancer cells. Moscatilin has been reported to exert proapoptotic effects in esophageal cancer, antimetastatic effects in lung and breast cancer, and anti-angiogenic activities against malignant tumors (16–19). The present study aimed to investigate whether the cytotoxicity of moscatilin on Panc-1 cells was associated with intracellular ROS production, and to determine the underlying mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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Moscatilin induces apoptosis of pancreatic cancer cells via reactive oxygen species and the JNK/SAPK pathway

Zhang

Fang

et al. 2017

Molecular Medicine Reports

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Moscatilin is a bibenzyl derivative extracted from the Dendrobium aurantiacum var. denneanum, which has traditionally been used as an immunomodulatory treatment in China. The present study was designed to determine whether moscatilin is a pro-apoptotic agent in pancreatic cancer, and to elucidate the underlying mechanisms. The apoptotic and anti-proliferative effects of moscatilin on pancreatic cancer cells were determined in vitro using biochemical assays, such as the MTT assay, colony formation assay, Hoechst staining and DNA fragmentation assay, and in vivo using Panc-1 pancreatic cancer xenografts. Western blotting was also conducted to evaluate the expression levels of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), Bcl2 homologous antagonist killer (Bak), caspase 3, cleaved-caspase 3, poly (ADP-ribose) polymerase, p-c-Jun N-terminal kinase (JNK)/stress-activated protein kinases (SAPK) and JNK/SAPK in response to moscatilin. We used DCFH-DA to detect the production of reactive oxygen species (ROS) induced by moscatilin. The present study demonstrated that moscatilin markedly inhibited pancreatic cancer cell viability and induced cell apoptosis in a concentration-dependent manner. Conversely, moscatilin did not affect the cell viability of human umbilical vein endothelial cells at the comparable dosage. Treatment with moscatilin suppressed clonogenicity of Panc-1 cells in a concentration-dependent manner. Furthermore, a decrease in Bcl2 expression, and an increase in the expression levels of Bak and Bax, was detected following treatment with moscatilin, resulting in an increase in the proapoptotic/anti-apoptotic expression ratio (Bax/Bcl2) in Panc-1 cells. Moscatilin also induced activation of the caspase-dependent mitochondrial apoptotic pathway. In addition, moscatilin enhanced cellular ROS production and induced activation of JNKSAPK signaling pathway. Conversely, pretreatment with the ROS scavenger N-acetylcysteine or the JNK/SAPK-specific inhibitor SP600125 prevented moscatilin-mediated reductions in cell viability. Furthermore, moscatilin inhibited tumor growth in nude mice bearing Panc-1 cells, without apparent toxicity. In conclusion, these results demonstrated that moscatilin may induce pancreatic cell apoptosis, and therefore may be considered a potential therapeutic agent for the treatment of pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Moscatilin induces apoptosis of pancreatic cancer cells via reactive oxygen species and the JNK/SAPK pathway

Zhang

Fang

et al. 2017

Molecular Medicine Reports

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“…Thus, 40 can be considered as a compound with a broad potential against esophageal cancer. [76] Recently, Yang et al reported the isolation and structural characterization of two dihydrostilbenoid derivatives, namely dendrocandins T (41), U (42), and B (43), together with other dihydrostilbenoids that displayed significant effects in the neurite outgrowthpromoting activity assay. [77] Gigantol (44) suppressed the migratory behavior of non-small cell lung cancer cells (NSCLC) H460 and H292 but did not show a similar effect on HaCat normal human keratocytes.…”

Section: Dihydrostilbenoids and Related Derivativesmentioning

confidence: 99%

“…Immunofluorescence studies revealed multipolar mitosis and multinucleation in cells, suggesting the development of mitotic catastrophe. Thus, 40 can be considered as a compound with a broad potential against esophageal cancer …”

Section: Introductionmentioning

confidence: 99%

Bioactive Secondary Metabolites from Orchids (Orchidaceae)

Sut

Maggi

Dall’Acqua

2017

Chemistry & Biodiversity

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The Orchidaceae family is the largest group of flowering plants in the Angiosperm monocotyledons spread on our planet. Its members, called orchids, are herbs or epiphytes with showy flowers distributed mainly in tropical regions. Several classes of phytoconstituents have been so far isolated from therapeutically-used orchids showing a great chemical diversity. Among them, phenolic derivatives have been studied for their biological activities, especially in the field of cancer, inflammation, and neurodegeneration. On the other hand, limited information has been so far obtained on the numerous alkaloids and terpenoids isolated from several orchid species. Recent articles revealed pronounced effects of some alkaloids on the CNS. Published literature on orchids that are used in traditional medicine has been reviewed in this work indicating a great potential of such organisms as source of chemical entities for the development of new drugs.

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“…The cells exit mitosis without cell division, forming a single giant cell with multi-nuclei and decondensed chromatin [27]. Moscatilin also produces the aforementioned changes in vitro [31]. This type of cell death could result from the alteration in the regulators of mitosis, including cell-cycle-specific kinases (e.g.…”

Section: Discussionmentioning

confidence: 99%

The Novel Thienopyrimidine Derivative, RP-010, Produces Its Efficacy in Prostate Cancer Cells by Inducing the Fragmentation of β-catenin

Amawi¹,

Hussein²,

Boddu³

et al. 2019

Preprint

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Thienopyrimidines are a versatile group of compounds that contain a biologically active pharmacophore and reported to have anticancer efficacy in vitro. Here, we report for the first time, that thieno[3,2-d]pyrimidine - based compounds, designated the RP series, have efficacy in prostate cancer cells. The lead compound, RP-010, was efficacious in PC3 and DU-145 prostate cancer (PC) cells (IC50< 1µM). The cytotoxicity of RP-010 was significantly lower in normal cells. RP-010 (0.5, 1, 2, and 4 µM) arrested prostate cancer cells in the G2 phase of the cell cycle, induced mitotic catastrophe and apoptotic signaling in both PC cell lines. Mechanistic studies suggested that RP-010 (1 and 2 µM) inhibits the wingless-type MMTV (Wnt)/β-catenin signaling pathway, mainly by inducing β-catenin fragmentation, while down regulating important proteins in the pathway, i.e. LRP-6, DVL3, and c-Myc. Interestingly, RP-010 (1 and 2 µM) induced the nuclear translocation of the negative feedback proteins, Naked 1 and Naked 2, in the signaling pathway. In addition, RP-010 (0.5, 1, 2, and 4 µM) significantly decreased the migration and invasiveness of PC cells in vitro. Finally, RP-010 did not produce significant toxic effects in zebrafish at concentrations up to 6 µM. In conclusion, RP-10 is a promising anticancer compound in metastatic prostate cancer and did not produce overt toxicity in an in vivo zebrafish model. Future mechanistic and efficacy studies are needed in-vivo to optimize the lead compound RP-010 for clinical use.

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Moscatilin Induces Apoptosis and Mitotic Catastrophe in Human Esophageal Cancer Cells

Cited by 30 publications

References 30 publications

Moscatilin induces apoptosis of pancreatic cancer cells via reactive oxygen species and the JNK/SAPK pathway

Moscatilin induces apoptosis of pancreatic cancer cells via reactive oxygen species and the JNK/SAPK pathway

Bioactive Secondary Metabolites from Orchids (Orchidaceae)

The Novel Thienopyrimidine Derivative, RP-010, Produces Its Efficacy in Prostate Cancer Cells by Inducing the Fragmentation of β-catenin

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Moscatilin Induces Apoptosis and Mitotic Catastrophe in Human Esophageal Cancer Cells

Cited by 30 publications

References 30 publications

Moscatilin induces apoptosis of pancreatic cancer cells via reactive oxygen species and the JNK/SAPK pathway

Moscatilin induces apoptosis of pancreatic cancer cells via reactive oxygen species and the JNK/SAPK pathway

Bioactive Secondary Metabolites from Orchids (Orchidaceae)

The Novel Thienopyrimidine Derivative, RP-010, Produces Its Efficacy in Prostate Cancer Cells by Inducing the Fragmentation of &beta;-catenin

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Resources

About

The Novel Thienopyrimidine Derivative, RP-010, Produces Its Efficacy in Prostate Cancer Cells by Inducing the Fragmentation of β-catenin