The apoptotic inducible effects of salicylic acid on hepatoma cell line: relationship with nitric oxide signaling

Liu, Yahui; Wang, Yong; Y, Hu; Ge, Shuxiong; Li, Keshi; Wang, Shuangshuang; Li, Li

doi:10.1007/s12079-017-0380-z

Cited by 8 publications

(5 citation statements)

References 34 publications

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“…For this reason, we analyzed a very strong apoptosis indicator, active caspase-3 protein levels by western blotting and we showed that there is a significant two-fold increase in active-caspase 3 levels of acibenzolar-S-methyltreated and MEK1/2 inhibited SH-SY5Y cells (Figures 3A and 3B). This result correlates with the results of the studies performed with human colorectal tumor cell lines and hepatoma cell line showing dose-and time-dependent apoptotic effect of SA (7,8), and also with the results of the study performed with A549 human lung cancer cells demonstrating the suppressing and apoptotic effect of SA on MAPK signaling (9). On the other hand, our result is inconsistent with the results of the study showing that inhibiting MEK1/2 signaling contributes to resistance to apoptosis in melanoma cells (10).…”

Section: Discussionsupporting

confidence: 89%

“…Furthermore, researchers examining the effect of SA on a hepatoma cell line have shown that SA can inhibit proliferation and induce apoptosis of the hepatoma cell line in a time and dose-dependent manner (7). In addition, in a study of human colorectal tumor cell lines, the effect of salicylate, aspirin metabolite, on these cell lines was determined.…”

Section: Introductionmentioning

confidence: 99%

“…To this end, several important studies have been performed and results showed that low dose aspirin which contains salicylic acid (SA) reduces the incidence and mortality of colorectal, breast, gastric, lung or other cancers (2)(3)(4)(5)(6). Furthermore, researchers examining the effect of SA on a hepatoma cell line have shown that SA can inhibit proliferation and induce apoptosis of the hepatoma cell line in a time and dose-dependent manner (7). In addition, in a study of human colorectal tumor cell lines, the effect of salicylate, aspirin metabolite, on these cell lines was determined.…”

Section: Introductionmentioning

confidence: 99%

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Acibenzolar-S-Methyl Inhibits MEK1/2 Signaling in SH-SY5Y Neuroblastoma Cells

Yildiz¹

2019

Eur J Biol

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Objective: Targeted cancer therapy using targeted cell proliferation inhibitors has become increasingly more critical. Studies conducted over the last decade have shown that non-steroidal drugs containing salicylic acid (SA) such as aspirin reduce mortality in many cancers. From this perspective, there are data suggesting SA as a potential inhibitor of the mitogenic MEK1/2 (mitogen-activated-protein-kinase, MAPK), extracellular-signal regulated-protein-kinase (ERK)) signaling, which could be highly effective in the prevention of proliferation in cancer. To date, no study has been conducted on the effect of SA on MEK1/2 signaling in neuroblastoma cells. Thus, the aim of this study is to reveal whether SA has an effect on MEK1/2 signaling in neuroblastoma cancer which is a frequent pediatric cancer with poor prognosis. Materials and Methods: The purpose of this study was to investigate whether a SA analog acibenzolar-S-methyl had an effect on the MEK1/2 signaling pathway and on cell viability in SH-SY5Y neuroblastoma cells by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) cell viability analysis and MEK1/2 and active caspase-3 detection by western blotting technique. Results: MTS cell viability test indicated that 10 mM acibenzolar-S-methyl reduces cell viability by 50%. Western blotting results of 10 mM acibenzolar-S-methyl-treated cells showed that MEK1/2 signaling was significantly inhibited in SH-SY5H cells. Besides, an increase in active-caspase-3 levels provided insight into acibenzolar-S-methyl's apoptotic effect which needs further morphological apoptotic data. Conclusion: Our research is the first to show that SA analog acibenzolar-S-methyl negatively affects MEK1/2 signaling causing the death of SH-SY5Y neuroblastoma cells. Our results can give insight not only into understanding the mechanisms of carcinogenesis but also into developing effective treatment methods.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acibenzolar-S-Methyl Inhibits MEK1/2 Signaling in SH-SY5Y Neuroblastoma Cells

Yildiz¹

2019

Eur J Biol

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“…A wide range of chemical entities possesses ·OH‐scavenging abilities, for instance isopropyl alcohol, cytosine, uracil, Tempo, GSH, and DMSO, among which a great proportion are biologically relevant . However, a reliable and robust method to quantify their reactivity is currently lacking, impeding the understanding of various fundamental processes in chemical and biological systems.…”

Section: Resultsmentioning

confidence: 99%

Synthesis and activity of a coumarin‐based fluorescent probe for hydroxyl radical detection

Zhang

Zhou

et al. 2019

Luminescence

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As a type of reactive oxygen species (ROS), hydroxyl radical (·OH) is closely associated with many kinds of diseases. The present study aimed to develo p a novel OH fluorescent probe based on coumarin, a new compound that has not been previously reported. This probe exhibited good linear range and selectivity for ·OHl, and is able to avoid interference from some metal ions and other kinds of ROS (H2O2, O2.‐, 1O2, and HClO). Meanwhile, this probe has been used to evaluate the ·OH‐scavenging efficiency of different compounds, such as isopropyl alcohol, cytosine, uracil, Tempo, Glutathione (GSH), and dimethyl sulfoxide (DMSO). Therefore, the present study shows that this probe not only can effectively measure the level of ·OH, but also can assess the ·OH‐scavenging efficiency of different compounds. Furthermore this current study suggested that following further optimization, this probe may be potentially applied in the diagnosis of oxidative stress in human body.

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“…Several cancer prevention properties of Aspirin are mediated by specific activities of salycilate (SA) affecting several cell processes conserved in eukaryotes, such as glucose metabolism 31 32 or apoptosis (e.g. see refs 33 34 and citations therein). So, it is not surprising that some of its established targets in mammals, e.g AMPK 31 , GCN2 35 , mTORC1 36 and HMGB1 37 , reveal key biological functions from yeast to man.…”

Section: Discussionmentioning

confidence: 99%

Antagonism between salicylate and the cAMP signal controls yeast cell survival and growth recovery from quiescence

Baroni¹,

Colombo²,

Martegani³

2018

Microb Cell

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Aspirin and its main metabolite salicylate are promising molecules in preventing cancer and metabolic diseases. S. cerevisiae cells have been used to study some of their effects: (i) salicylate induces the reversible inhibition of both glucose transport and the biosyntheses of glucose-derived sugar phosphates, (ii) Aspirin/salicylate causes apoptosis associated with superoxide radical accumulation or early cell necrosis in MnSOD-deficient cells growing in ethanol or in glucose, respectively. So, treatment with (acetyl)-salicylic acid can alter the yeast metabolism and is associated with cell death. We describe here the dramatic effects of salicylate on cellular control of the exit from a quiescence state. The growth recovery of long-term stationary phase cells was strongly inhibited in the presence of salicylate, to a degree proportional to the drug concentration. At high salicylate concentration, growth reactivation was completely repressed and associated with a dramatic loss of cell viability. Strikingly, both of these phenotypes were fully suppressed by increasing the cAMP signal without any variation of the exponential growth rate. Upon nutrient exhaustion, salicylate induced a premature lethal cell cycle arrest in the budded-G2/M phase that cannot be suppressed by PKA activation. We discuss how the dramatic antagonism between cAMP and salicylate could be conserved and impinge common targets in yeast and humans. Targeting quiescence of cancer cells with stem-like properties and their growth recovery from dormancy are major challenges in cancer therapy. If mechanisms underlying cAMP-salicylate antagonism will be defined in our model, this might have significant therapeutic implications.

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The apoptotic inducible effects of salicylic acid on hepatoma cell line: relationship with nitric oxide signaling

Cited by 8 publications

References 34 publications

Acibenzolar-S-Methyl Inhibits MEK1/2 Signaling in SH-SY5Y Neuroblastoma Cells

Acibenzolar-S-Methyl Inhibits MEK1/2 Signaling in SH-SY5Y Neuroblastoma Cells

Synthesis and activity of a coumarin‐based fluorescent probe for hydroxyl radical detection

Antagonism between salicylate and the cAMP signal controls yeast cell survival and growth recovery from quiescence

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