Jasmonates Induce Apoptosis and Cell Cycle Arrest in Non-Small Cell Lung Cancer Lines

Yeruva, Laxmi; Pierre, Keon J.; Carper, Stephen W.; Elegbede, J. Abiodun; Toy, Brian C.; Wang, Robert C.

doi:10.1080/01902140601059604

Cited by 22 publications

(14 citation statements)

References 28 publications

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“…Alltogether, these results suggest that OPDA may have therapeutic effects not only in breast cancer cells but also in other tumors, where increased nuclear b-catenin expression has been attributed to early carcinogenesis. Previous studies showed that jasmonic acid, a betaoxidation product of OPDA in plants, causes growth arrest, apoptosis and differentiation in various human tumor cells at millimolar concentrations [39][40][41]. This effect has been associated with induction of JNK, MAPK and AP-1 activities.…”

Section: Discussionmentioning

confidence: 95%

A plant oxylipin, 12-oxo-phytodienoic acid, inhibits proliferation of human breast cancer cells by targeting cyclin D1

Altiok

Mezzadra

Patel

et al. 2007

Breast Cancer Res Treat

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Cyclin D1 overexpression has been associated with poor prognosis and resistance to therapy in human breast cancer. Thus, the development of therapeutic agents that selectively target cyclin D1 activity is of clinical interest. This study demonstrates that 12-oxo-phytodienoic acid (OPDA), a phytohormone with critical functions in growth and development in plants, induces growth arrest in MDA-MB-231 and T47D breast cancer cells. In response to OPDA treatment, the human breast cancer cell lines exhibit a progressive decline in cyclin D1 expression, which is tightly associated with the accumulation of hypophosphorylated form of the retinoblastoma protein (Rb) and G1 arrest. The decrease in cyclin D1 protein expression accompanies a dramatic decline in nuclear but not membranous beta-catenin expression and activation of glycogen synthase kinase-3-beta (GSK3beta) caused by inhibition of its serine-9 phosphorylation. The proteasome inhibitor MG132 blocks OPDA-mediated decrease in cyclin D1. In addition, the overexpression of T286A, a cyclin D1 mutant which is refractory to phosphorylation by GSK3beta and proteosomal degradation, is resistant to OPDA-mediated Rb dephosphorylation as well as G(1) cell cycle arrest. Thus, our results demonstrate that degradation of cyclin D1 protein is a key event in OPDA induced growth inhibition in breast cancer cells. These data provide the basic foundation for future efforts to develop OPDA-based approaches in the prevention and treatment of breast cancer and other types of cancer.

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Section: Discussionmentioning

confidence: 95%

A plant oxylipin, 12-oxo-phytodienoic acid, inhibits proliferation of human breast cancer cells by targeting cyclin D1

Altiok

Mezzadra

Patel

et al. 2007

Breast Cancer Res Treat

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“…JAs also increased the life span of T-cell lymphoma-bearing mice [17]. Thereafter JAs, including MJ and related synthetic analogs, were found to inhibit in vitro cancer cell proliferation and to induce cell death in other human and murine cancer cell types [16, 19–24], including human breast [15, 25], cervix [26–29], colon [30, 31], colorectal [32], gastric [33], hepatoma [34, 35], lung [19, 36, 37], lymphoma [15, 17, 18, 38], melanoma [15, 30, 39, 40], myeloid leukemia [41, 42], neuroblastoma [43–45], prostate [15, 46–48], and sarcoma [49] cancer cells (Table 1). Other results have shown that JAs and their synthetic derivates exerted selected cytotoxic effects in vivo towards metastatic melanoma [21, 39] and inhibited angiogenesis at high doses (it was the reverse at low doses) in the chorioallantoic membrane (CAM) of chicken embryo [40] (Table 2).…”

Section: Effects Of Jasmonates On Mammalian Cancer Cellsmentioning

confidence: 99%

“…JAs (mainly MJ) have been found to arrest cell cycle of different cancer cell types at different phases (Table 1): G 0 /G 1 , in human acute lymphoblastic leukemia Molt-4 [14, 38] and human neuroblastoma SK-N-SH, BE(2)-C [45]; G 0 /G 1 -S in human breast MCF-7 and melanocytic MDA-MB-435 cancer cells [25, 74]; S, in human neuroblastoma BE(2)-C [43]; S-G 2 /M, in human adenocarcinoma colon HT-39 [31]; G 2 /M, in nonsmall cell lung cancer (NSCLC) lines A549 and H520 [37], human neuroblastoma SH-SY5Y [44], human cervical carcinoma, and HeLa cells [27]. At 0.1 mM, MJ arrested in vitro human umbilical vein endothelial cells (HUVEC) at G 1 [40].…”

Section: Effects Of Jasmonates On Mammalian Cancer Cellsmentioning

confidence: 99%

“…In some cases of cell cycle arrest, MJs have been found to upregulate p21 [37] whereas in others to downregulate survivin mRNA and protein levels [43–45] (Table 1). Survivin is an important member of the inhibitor of apoptosis protein (IAP) family that also regulates entrance of the cell cycle to the M phase and is overexpressed in cancer cells acting linking both regulation of the cell cycle and inhibition of apoptosis [79].…”

Section: Effects Of Jasmonates On Mammalian Cancer Cellsmentioning

confidence: 99%

“…Nonapoptotic cell death could be the consequence of the severe bioenergetic damages induced by the direct interaction of MJ with mitochondria, leading to increased ROS levels, inhibition of ATP synthesis, and ATP depletion [20, 30]. Jasmonates, including MJ and some of its analogs, have been found to be strongly proapoptotic in vitro in different types of cancer cells, by both the extrinsic and the intrinsic pathway (Table 1), with no or little cytotoxicity to normal cells [15, 25, 36, 37, 44, 45]. Thus, MJ induced the expression of TNFR1 in human breast MCF-7 and MDA-MB-435 cells [25, 74] and in hormone-independent human prostate PC-3 and DU 145 cancer cells promoting apoptosis by the extrinsic pathway in these cells [48].…”

Section: Effects Of Jasmonates On Mammalian Cancer Cellsmentioning

confidence: 99%

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Methyl Jasmonate: Putative Mechanisms of Action on Cancer Cells Cycle, Metabolism, and Apoptosis

Cesari

Carvalho

Rodrigues

et al. 2014

International Journal of Cell Biology

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Methyl jasmonate (MJ), an oxylipid that induces defense-related mechanisms in plants, has been shown to be active against cancer cells both in vitro and in vivo, without affecting normal cells. Here we review most of the described MJ activities in an attempt to get an integrated view and better understanding of its multifaceted modes of action. MJ (1) arrests cell cycle, inhibiting cell growth and proliferation, (2) causes cell death through the intrinsic/extrinsic proapoptotic, p53-independent apoptotic, and nonapoptotic (necrosis) pathways, (3) detaches hexokinase from the voltage-dependent anion channel, dissociating glycolytic and mitochondrial functions, decreasing the mitochondrial membrane potential, favoring cytochrome c release and ATP depletion, activating pro-apoptotic, and inactivating antiapoptotic proteins, (4) induces reactive oxygen species mediated responses, (5) stimulates MAPK-stress signaling and redifferentiation in leukemia cells, (6) inhibits overexpressed proinflammatory enzymes in cancer cells such as aldo-keto reductase 1 and 5-lipoxygenase, and (7) inhibits cell migration and shows antiangiogenic and antimetastatic activities. Finally, MJ may act as a chemosensitizer to some chemotherapics helping to overcome drug resistant. The complete lack of toxicity to normal cells and the rapidity by which MJ causes damage to cancer cells turn MJ into a promising anticancer agent that can be used alone or in combination with other agents.

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An Update on Core Jasmonate Signalling Networks, Physiological Scenarios, and Health Applications

Pérez‐Salamó

Krasauskas

Gates

et al. 2019

Annual Plant Reviews Online

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Jasmonic acid, its precursors in the biosynthetic pathway and derivatives are lipid‐derived signalling molecules. Together with other plant hormones, they regulate responses to stress (biotic and abiotic), mediate defence (against pathogens and herbivores), and a plethora of processes including growth and reproductive development in different plant species. The discovery of jasmonates is more recent than that of auxin, abscisic acid, cytokinins, gibberellic acid, ethylene, and salicylic acid; however, their role in regulating plant developmental plasticity is second to none. Since the 1990s, research made substantial advances and added to the crosstalk with the abovementioned other hormones and signalling pathways. Building on the knowledge of over two decades, an update on the research in JAs signalling components regulating plant responses to developmental and environmental cues is provided here. Information in Arabidopsis thaliana is integrated with reports on other plants. Recent findings in the regulation of plant responses to biotics and abiotic stressors and evidence implicating JAs in the regulation of the trade‐off between growth and stress will be reported. Health applications for JAs and JAs‐induced secondary metabolism, bridging the gap between biotechnology and traditional medicine, will illustrate the practical and societal relevance of investigating the functions of such compounds.

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Jasmonates Induce Apoptosis and Cell Cycle Arrest in Non-Small Cell Lung Cancer Lines

Cited by 22 publications

References 28 publications

A plant oxylipin, 12-oxo-phytodienoic acid, inhibits proliferation of human breast cancer cells by targeting cyclin D1

A plant oxylipin, 12-oxo-phytodienoic acid, inhibits proliferation of human breast cancer cells by targeting cyclin D1

Methyl Jasmonate: Putative Mechanisms of Action on Cancer Cells Cycle, Metabolism, and Apoptosis

An Update on Core Jasmonate Signalling Networks, Physiological Scenarios, and Health Applications

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