The anticancer plant stress-protein methyl jasmonate induces activation of stress-regulated c-Jun N-terminal kinase and p38 protein kinase in human lymphoid cells

Rotem, Ronit; Fingrut, Orit; Moskovitz, Jackob; Flescher, Eliezer

doi:10.1038/sj.leu.2403107

Cited by 29 publications

(26 citation statements)

References 8 publications

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“…Methyl jasmonate induced death in breast and prostate carcinoma cells, as well as in melanoma, lymphoma, and leukemia cells (4). Furthermore, we determined that jasmonates are capable of killing cancer cells in a manner independent of cellular mRNA transcription, protein translation (5), and p53 expression. 3 Finally, methyl jasmonate significantly increased the life span of lymphomabearing mice (4).…”

Section: Introductionmentioning

confidence: 92%

Jasmonates: Novel Anticancer Agents Acting Directly and Selectively on Human Cancer Cell Mitochondria

et al. 2005

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Section: Introductionmentioning

confidence: 92%

Jasmonates: Novel Anticancer Agents Acting Directly and Selectively on Human Cancer Cell Mitochondria

et al. 2005

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“…A recent report shows that MJ induces activation of stress-regulated c-Jun N-terminal kinase and p38 protein kinase in lymphoid cells. 31 Further experimentation is necessary to understand the role of MAPKs on anticancer action of MJ.…”

Section: Discussionmentioning

confidence: 99%

Induction of differentiation of human myeloid leukemia cells by jasmonates, plant hormones

et al. 2004

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Some regulators of plant growth and differentiation have been shown to induce the differentiation of several human myeloid leukemia cells, and might be effective as differentiation inducers to control acute myelogenous leukemia cells. In this study, the growth-inhibiting and differentiation-inducing effects of jasmonates on human myeloid leukemia cells were examined. Several myeloid leukemia cells were cultured with methyl jasmonate (MJ) and its derivatives. Cell differentiation was determined by nitroblue tetrazolium-reducing activity, morphological changes, a-naphthyl acetate esterase activity and expression of differentiation-associated surface antigens. MJ induced both monocytic and granulocytic differentiation of HL-60 cells. MJ activated mitogen-activated protein kinase (MAPK) in the cells before causing myelomonocytic differentiation. MAPK activation was necessary for MJ-induced differentiation, since PD98059, an inhibitor of MAPK kinase, suppressed the differentiation induced by MJ. MJ also induced the differentiation of other human leukemia cell lines. Introduction of a double bond at the 4,5-position greatly enhanced the differentiationinducing activity of MJ. MJ and its derivatives potently induce the differentiation of some myelomonocytic leukemia cells. One novel derivative is a particularly promising therapeutic agent for the treatment of leukemia.

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“…JAs also are implicated in the control of plant responses to abiotic stimuli such as mechanical stress (Weiler et al, 1993), salt stress (Dombrowski, 2003), UV irradiation (Conconi et al, 1996), and ozone exposure (Rao et al, 2000). The ability of JAs to regulate gene expression in plant, insect (Li et al, 2002c), and mammalian (Rotem et al, 2003) cells indicates that some components of this lipid-based signaling system may be conserved in diverse biological systems.…”

Section: Introductionmentioning

confidence: 99%

The Tomato Homolog of CORONATINE-INSENSITIVE1 Is Required for the Maternal Control of Seed Maturation, Jasmonate-Signaled Defense Responses, and Glandular Trichome Development[W]

et al. 2004

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Jasmonic acid (JA) is a fatty acid-derived signaling molecule that regulates a broad range of plant defense responses against herbivores and some microbial pathogens. Molecular genetic studies in Arabidopsis have established that JA also performs a critical role in anther and pollen development but is not essential for other developmental aspects of the plant's life cycle. Here, we describe the phenotypic and molecular characterization of a sterile mutant of tomato ( jasmonic acidinsensitive1 [ jai1 ]) that is defective in JA signaling. Although the mutant exhibited reduced pollen viability, sterility was caused by a defect in the maternal control of seed maturation, which was associated with the loss of accumulation of JAregulated proteinase inhibitor proteins in reproductive tissues. jai1 plants exhibited several defense-related phenotypes, including the inability to express JA-responsive genes, severely compromised resistance to two-spotted spider mites, and abnormal development of glandular trichomes. We demonstrate that these defects are caused by the loss of function of the tomato homolog of CORONATINE-INSENSITIVE1 (COI1), an F-box protein that is required for JA-signaled processes in Arabidopsis. These findings indicate that the JA/COI1 signaling pathway regulates distinct developmental processes in different plants and suggest a role for JA in the promotion of glandular trichome-based defenses.

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The anticancer plant stress-protein methyl jasmonate induces activation of stress-regulated c-Jun N-terminal kinase and p38 protein kinase in human lymphoid cells

Cited by 29 publications

References 8 publications

Jasmonates: Novel Anticancer Agents Acting Directly and Selectively on Human Cancer Cell Mitochondria

Jasmonates: Novel Anticancer Agents Acting Directly and Selectively on Human Cancer Cell Mitochondria

Induction of differentiation of human myeloid leukemia cells by jasmonates, plant hormones

The Tomato Homolog of CORONATINE-INSENSITIVE1 Is Required for the Maternal Control of Seed Maturation, Jasmonate-Signaled Defense Responses, and Glandular Trichome Development[W]

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