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methyl jasmonate/syöpä
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 90 tuloksia
Delayed cytotoxic effects of methyl jasmonate and cis-jasmone induced apoptosis in prostate cancer cells.
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Advanced prostate cancer cells are typically hormone independent, resistant to apoptosis and do not respond to chemotherapeutic agents. The ability of methyl jasmonate (MJ) and cis-jasmone (CJ) to inhibit growth in hormone independent prostate cancer cell lines, PC-3 and DU-145, was evaluated. CJ
Methyl jasmonate reduces the survival of cervical cancer cells and downregulates HPV E6 and E7, and survivin.
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The present study further investigated the mode of action of methyl jasmonate (MJ) in different cervical cancer cell lines. We show that in addition to the short term cytotoxicity, MJ effectively reduced the survival of cervical cancer cells (clonogenicity assays). MJ induced apoptosis in all
Design and production of methyl jasmonate nanoemulsions using experimental design technique and evaluation of its anti-cancer efficacy.
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Methyl jasmonate (MJ), a plant-derived stress hormone, has been shown to be a promising anti-cancer agent with high selectivity toward cancerous cells. The aim of the present study was to design a MJ loaded nanoemulsion (NE) to overcome the low MJ water solubility and also improve its anti-cancer
Methyl jasmonate sensitizes human bladder cancer cells to gambogic acid-induced apoptosis through down-regulation of EZH2 expression by miR-101.
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OBJECTIVE
Gambogic acid (GA) and methyl jasmonate (MJ) are increasingly being recognized as novel natural anticancer compounds. Here, we investigated the antitumour effects of GA in combination with MJ on human bladder cancer cells.
METHODS
Cell viability was detected by cell counting kit-8 assay.
Methyl jasmonate and its potential in cancer therapy.
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Methyl jasmonate (MeJa) is a naturally occurring hydrophobic oxylipin phytohormone. Early findings obtained from cancer cell lines suggest that MeJa is endowed with anticancer capabilities. It has been recently proposed that MeJa represents a novel agent that exhibits direct and selective actions
EZH2 inhibition promotes methyl jasmonate-induced apoptosis of human colorectal cancer through the Wnt/β-catenin pathway.
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Methyl jasmonate potentially induces the differentiation of human myeloid leukemia cells and inhibits their proliferation; it may induce the differentiation and apoptosis of human lymphocytic leukemia cells, but does not exert a damaging effect on normal lymphocytes. In the present study, the
Methyl jasmonate induces the apoptosis of human colorectal cancer cells via downregulation of EZH2 expression by microRNA‑101.
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Methyl jasmonate is found universally in the plant kingdom and functions to regulate plant growth and development, as well as in stress responses through signal transduction pathways. The present study aimed to investigate the anticancer effect of methyl jasmonate on SW620 human colorectal cancer
Methyl jasmonate: putative mechanisms of action on cancer cells cycle, metabolism, and apoptosis.
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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
Methyl jasmonate: a plant stress hormone as an anti-cancer drug.
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Jasmonates act as signal transduction intermediates when plants are subjected to environmental stresses such as UV radiation, osmotic shock and heat. In the past few years several groups have reported that jasmonates exhibit anti-cancer activity in vitro and in vivo and induce growth inhibition in
Methyl jasmonate induces cell death with mixed characteristics of apoptosis and necrosis in cervical cancer cells.
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In the present study the effectiveness of methyl jasmonate (MJ) against cervical cancer cell lines was investigated. We show that MJ is cytotoxic to a range of cervical cancer lines including SiHa, CaSki and HeLa that carry human papillomavirus (HPV) DNA and wild type p53, and C33A that is negative
Enhanced killing of cervical cancer cells by combinations of methyl jasmonate with cisplatin, X or alpha radiation.
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Current therapies for treatment of advanced cervical cancer involve the use of cisplatin, often in combination with radiotherapy. These treatments do not lead to a high survival rate and furthermore, serious side effects are dose-limiting factors. Methyl jasmonate (MJ) was recently identified as
Cooperative cytotoxicity of methyl jasmonate with anti-cancer drugs and 2-deoxy-D-glucose.
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The anti-cancer agent methyl jasmonate (MJ) acts in vitro and in vivo against various cancer cell lines, as well as leukemic cells from chronic lymphocytic leukemia (CLL) patients. Given the importance of multi-agent combinations in cancer chemotherapy, the purpose of this study was to identify
Methyl jasmonate leads to necrosis and apoptosis in hepatocellular carcinoma cells via inhibition of glycolysis and represses tumor growth in mice.
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Methyl jasmonate has recently been found to have anti-cancer activity. Methyl jasmonate detached hexokinase 2 from a voltage dependent anion channel causing a reduction in mitochondrial transmembrane potential that led to the release of cytochrome C and apoptosis inducing factor resulting in
Synthesis of novel methyl jasmonate derivatives and evaluation of their biological activity in various cancer cell lines.
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Warburg hypothesized that the energy consumption of cancer cells is different than the normal cells. When compared to normal conditions, cancer cells do not undergo tricarboxylic acid (TCA) cycle therefore resulting in more lactate in the cells. Glycolysis pathway is a way of cancer cells to provide
Effect of methyl jasmonate and 3-bromopyruvate combination therapy on mice bearing the 4 T1 breast cancer cell line.
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Cancer cells apply the Warburg pathway to meet their increased metabolic demands caused by their rapid growth and proliferation and also creates an acidic environment to promote cancer cell invasion. 3-bromopyruvate (3-BrP) as an anti-cancer agent disrupts glycolytic pathway. Moreover, one of the
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