Moscatilin, a bibenzyl derivative from the orchid Dendrobium moscatum

Majumder, P.L.; Sen, R. N.

doi:10.1016/s0031-9422(00)81777-x

Cited by 94 publications

(48 citation statements)

References 8 publications

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“…To investigate the role of p53 in moscatilininduced apoptosis, we examined downstream effectors and the phosphorylation state of p53 in HCT-116 cells. Our results show that moscatilin induced an up-regulation and phosphorylation of p53 at Ser 15 , with a concomitant increase in the protein levels of p21 WAF1/CIP1 (Fig. 5C).…”

Section: Resultssupporting

confidence: 54%

“…Thus, triggering this pathway is a potential approach to anticancer therapy. Moscatilin induced an early DNA double-strand break (1 hour) and subsequently caused H2AX phosphorylation as well as up-regulated and activated p53 by phosphorylation at Ser 15 , which caused induction of p21 WAF1/CIP1 . This suggests that the , and g-H2AX protein expression.Whole-cell lysates were separated and detected using Western blot analysis.…”

Section: Discussionmentioning

confidence: 99%

“…Monoclonal antibody against caspase-3 was from Imgenex. Antibodies to caspase-8, caspase-9, phosphorylated JNK, JNK, phosphorylated c-Jun, phosphorylated H2AX (Ser 139 ), phosphorylated p53 (Ser 15 ), and p53 were from Cell Signal Technology. Antia-tubulin IgG was from Serotec Product.…”

Section: Methodsmentioning

confidence: 99%

“…Moscatilin (4,4 ¶-dihydroxy-3,3 ¶,5-trimethoxybibenzyl) is a bibenzyl component derived from the India orchid Dendrobrium moscatum (15) and the stem of Dendrobrium loddigesii (16).…”

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confidence: 99%

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Moscatilin Induces Apoptosis in Human Colorectal Cancer Cells: A Crucial Role of c-Jun NH2-Terminal Protein Kinase Activation Caused by Tubulin Depolymerization and DNA Damage

Chen

Pan

Guh

et al. 2008

Clinical Cancer Research

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Purpose: To study the effect of moscatilin (purified from the stem of orchid Dendrobrium loddigesii) on the proliferation of human colorectal cancer HCT-116 cells in vitro and in vivo. Experimental Design: The growth inhibition of moscatilin was screened on several human cancer cell lines. The effect of moscatilin on tubulin was detected in vitro. Following moscatilin treatment on HCT-116 cells, c-Jun NH 2 -terminal protein kinase (JNK) and caspase activation was studied by Western blot analysis, and DNA damage was done by Comet assay. Specific JNK inhibitor SP600125 was cotreated to reverse moscatilin-induced apoptosis. Tumor growth inhibition of moscatilin was done on HCT-116 xenograft models. Results: Moscatilin induced a time-dependent arrest of the cell cycle at G 2 -M, with an increase of cells at sub-G 1 . Moscatilininhibited tubulin polymerization, suggesting that it might bind to tubulins. Moscatilin also induced the phosphorylation ofJNK1/2. SP600125 significantly inhibited the activation of caspase-9 and caspase-3 and the subsequent moscatilin-induced apoptosis. The data suggest that JNK activation may contribute to moscatilin-mediated apoptosis signaling. A parallel experiment showed that SP600125 significantly inhibitsTaxol-and vincristine-induced HCT-116 cell apoptosis. This suggests that the JNK activation may be a common mechanism for tubulinbinding agents. Moreover, moscatilin induces DNA damage, phosphorylation of H2AX and p53, and up-regulation of p21. Our HCT-116 xenograft models show the in vivo efficacy of moscatilin. Conclusions: In summary, our results suggest that moscatilin induces apoptosis of colorectal HCT-116 cells via tubulin depolymerization and DNA damage stress and that this leads to the activation of JNK and mitochondria-involved intrinsic apoptosis pathway.

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Section: Resultssupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…Moscatilin (4,4 ¶-dihydroxy-3,3 ¶,5-trimethoxybibenzyl) is a bibenzyl component derived from the India orchid Dendrobrium moscatum (15) and the stem of Dendrobrium loddigesii (16).…”

mentioning

confidence: 99%

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