Luteolin sensitizes tumor necrosis factor-α-induced apoptosis in human tumor cells

Shi, Rui; Ong, Choon Nam; Shen, Han‐Ming

doi:10.1038/sj.onc.1208046

Cited by 96 publications

(85 citation statements)

References 53 publications

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“…Moreover, previous reports have shown c-myc gene was amplification and overexpression in esophageal cancer cell lines (Jones et al, 1993;Kanda et al, 1994). Although, it has reported luteolin could not inhibit myc expression in both cervical and colorectal cancer cells (Shi et al, 2004), in our study, luteolin downregulated the mRNA level of c-myc and decreased the protein expression of c-myc on Eca109 cells.…”

Section: Discussioncontrasting

confidence: 68%

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

Wang¹,

Wang²,

Huang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Luteolin is a plant flavonoid which exhibits anti-oxidative, anti-inflammatory and anti-tumor effects. However, the antiproliferative potential of luteolin is not fully understood. In this study, we investigated the effect of luteolin on cell cycling and apoptosis in human esophageal squamous carcinoma cell line Eca109 cells. MTT assays showed that luteolin had obvious cytotoxicity on Eca109 with an IC 50 of 70.7±1.72μM at 24h. Luteolin arrested cell cycle progression in the G0/G1 phase and prevented entry into S phase in a dose-and time-dependent manner. as assessed by FCM. Luteolin induced apoptosis of Eca109 cells was demonstrated by AO/EB staining assay and annexin V-FITC/PI staining. Moreover, luteolin downregulated the expression of cyclin D1, survivin and c-myc, and it also upregulated the expression of p53, in line with the fact that luteolin was able to inhibit Eca109 cell proliferation.

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Section: Discussioncontrasting

confidence: 68%

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

Wang¹,

Wang²,

Huang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Several reports indicate an NF-kB-dependent negative regulation of JNK activation. [37][38][39][40] JNK is a member of the mitogen-activated protein kinase family and is identified as three protein kinases, JNK1, JNK2 and a neuronal-specific form JNK3. In NIH3T3 cells, TNFa activates both NF-kB and JNK pathways, which is consistent with previous studies on TNFa signaling.…”

Section: Discussionmentioning

confidence: 99%

Novel synergistic mechanism for sst2 somatostatin and TNFα receptors to induce apoptosis: crosstalk between NF-κB and JNK pathways

et al. 2006

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Somatostatin is a multifunctional hormone that modulates cell proliferation, differentiation and apoptosis. Mechanisms for somatostatin-induced apoptosis are at present mostly unsolved. Therefore, we investigated whether somatostatin receptor subtype 2 (sst2) induces apoptosis in the nontransformed murine fibroblastic NIH3T3 cells. Somatostatin receptor subtype 2 expression induced an executioner caspase-mediated apoptosis through a tyrosine phosphatase SHP-1 (Src homology domain phosphatase-1)-dependent stimulation of nuclear factor kappa B (NF-jB) activity and subsequent inhibition of the mitogenactivated protein kinase JNK. Tumor necrosis factor a (TNFa) stimulated both NF-jB and c-Jun NH2-terminal kinase (JNK) activities, which had opposite action on cell survival. Importantly, sst2 sensitized NIH3T3 cells to TNFa-induced apoptosis by (1) upregulating TNFa receptor protein expression, and sensitizing to TNFa-induced caspase-8 activation; (2) enhancing TNFamediated activation of NF-jB, resulting in JNK inhibition and subsequent executioner caspase activation and cell death. We have here unraveled a novel signaling mechanism for a G protein-coupled receptor, which directly triggers apoptosis and crosstalks with a death receptor to enhance death ligand-induced apoptosis. Somatostatin is a regulatory peptide which is mostly expressed in the central and peripheral nervous system, in the gastro-intestinal tract and in the pancreas. Somatostatin acts via a family of five G protein-coupled receptors (GPCR), somatostatin receptor subtypes 1-5 (sst1-sst5) that are variably expressed throughout numerous tissues ranging from the central nervous system to the endocrine and immune systems. 1 Somatostatin or its analogues promote growth inhibition of various normal and tumor cells, both in vitro and in vivo. Somatostatin affects cell growth indirectly by inhibiting either trophic or growth factor synthesis and/or secretion, or their respective intracellular pathways. Somatostatin antiproliferative action also results from a direct blockade of cell cycle and/or induction of apoptosis. 2 Whereas somatostatin effect on cell cycle arrest has been extensively studied, mechanisms for somatostatin-induced apoptosis and receptor subtype implication are only partially elucidated. Somatostatin has been shown to induce cell death in both normal and tumoral cell models 3-9 . Among the five somatostatin receptors, sst3 and sst2 have been found to play a critical role in somatostatin-induced apoptosis of normal and tumor cells, respectively. 3,5,10 Mechanisms for somatostatin apoptotic action were shown to rely on the mitochondrial pathway through activation either of sst2 or sst3. However, signaling pathways coupling sst2 receptor to apoptosis have been partially elucidated.We have previously demonstrated that expression of sst2 in the nontransformated murine fibroblastic NIH3T3 cells results in a cell growth inhibition, which was dependent on the activation of the tyrosine phosphatase Src homology domain phosphatase-1 (SHP-1). 11 sst2...

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“…Cells were grown in every other well of a 384-well NUNC sterile, clear plate (25,000 cells/well, 25 µL/well) for 18 h. Solutions of the carbohydrates at the indicated concentrations (0.01 -4000 µM in sterile PBS) were pre-incubated with TNF-α (1 µL/well of a 125 ng/mL solution in sterile PBS) at rt. After 2h, the solutions were added to the cells and incubated for 18 h. At this time, caspase 3/7 activity was analyzed as described by Shi et al 8 …”

Section: S6mentioning

confidence: 99%

Discovery of a TNF-α Antagonist Using Chondroitin Sulfate Microarrays

2006

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Conjugation of CS Oligosaccharides to 1,2-(Bisaminooxy)ethane for Microarray ProductionOzonolysis of the anomeric allyl group and linkage of CS compounds 1-4 1,2 to 1,2-(bisaminooxy)ethane 3 proceeded as follows: oligosaccharide (0.51 µmol) was dissolved in MeOH (500 µL) and cooled to -78 °C. O 3 was bubbled through the reaction until a blue color persisted (1 min). The reaction was then purged with N 2 until colorless, quenched with Ph 3 P beads (3 mg), and gradually warmed to rt over 12 h. It was filtered and the product concentrated to afford the desired aldehyde as a white solid. The aldehyde (0.51 µmol) was then reacted for 14 h at rt with 1,2-(bisaminooxy)ethane hydrochloride (1.4 mg, 15 µmol) that had been dissolved in H 2 O (100 µL) and pH adjusted to 5.0 with 1 M NaOH. The resulting oxime product was purified using a SepPak C18 column (500 mg, H 2 O) and Sephadex G-10 (CS-E The relative concentrations of the aminooxy oligosaccharides were calibrated to one another using the carbazole assay for uronic acid residues. 4 Briefly, the acid borate reagent (1.5 mL of 0.80 g sodium tetraborate, 16.6 mL H 2 O, and 83.3 mL H 2 SO 4 ) was added to 20-mL glass vials with Teflon caps. The Carbohydrate MicroarraysSolutions of the aminooxy oligosaccharides (in 300 mM NaH 2 PO 4 , pH 5.0, 10 µL/well in a 384-well plate) were arrayed on Hydrogel Aldehyde slides (NoAb Biodiscoveries) by using a Microgrid II arrayer (Biorobotics) to deliver sub-nanoliter volumes at rt and 50% humidity. Concentrations of carbohydrates ranged from 0 -500 µM. The resulting arrays were incubated in a 70% humidity chamber at rt for 12 h and then stored in a low humidity, dust-free dessicator. The pH and reaction time were Non-specific attachment of CS oligosaccharides lacking the aminooxy linker (e.g., compounds 1-4) was not observed. Prior to use, the arrays were outlined with a hydrophobic pen (Super Pap Pen, Research Products International) to create a boundary for the protein treatments and rinsed three times with H 2 O. The slides were then blocked by treatment with NaBH 4 (125 mg) in 140 mM NaCl, 2.7 mM KCl, 5.4 mM Na 2 HPO 4 , and 1.8 mM KH 2 PO 4 (phosphate buffered saline, PBS, 50 mL) at rt for 5 min with gentle rocking and washed five times for 3 min with PBS. For all incubations, the slides were placed in a covered pipette tip box. Human TNF-α (Peprotech), FGF-1 (R&D Systems; both reconstituted to 2 µM in 0.1% Triton X-100 in PBS), cell culture supernatant containing monoclonal anti-CS-A antibody, or cell culture supernatant containing monoclonal anti-CS-E antibody (both 1:1 in 0.1% Triton X-100 in PBS) were spotted onto the slides in 250 µL quantities, and incubated statically at rt for 2 h. The slides were then washed as previously described and incubated with the appropriate primary antibody [anti-TNF-α (Peprotech) or anti-FGF-1 (R&D Systems); 1:1000 in 0.1% Triton X-100 in PBS] for 2 h at rt with gentle rocking. Following the incubation, the slides were washed as previously described and treated in the dark at rt with a seconda...

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Luteolin sensitizes tumor necrosis factor-α-induced apoptosis in human tumor cells

Cited by 96 publications

References 53 publications

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

Novel synergistic mechanism for sst2 somatostatin and TNFα receptors to induce apoptosis: crosstalk between NF-κB and JNK pathways

Discovery of a TNF-α Antagonist Using Chondroitin Sulfate Microarrays

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