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Find video protocols related to scientific articles indexed in Pubmed.
Chemomodulatory efficacy of lycopene on antioxidant enzymes and carcinogen-induced cutaneum carcinoma in mice.
Food Funct
PUBLISHED: 05-01-2014
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Oxidative stress has been implicated in various pathological processes, including skin tumourigenesis. Cutaneum carcinoma is commonly responsible for considerable morbidity and mortality, and treatments have not progressed substantially in recent years. Alternative strategies, such as chemoprevention, are being considered. In this study, we investigated the chemomodulatory potential of lycopene against 9,10-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative stress and skin carcinogenesis in female ICR mice. Pretreatment with lycopene at various doses significantly delayed tumour formation and growth. These treatments markedly reduced the tumour incidence and tumour volume. Moreover, lycopene inhibited the formation of reactive oxygen species and malondialdehyde, prevented the loss of glutathione, and affected the activities of a battery of oxidant enzymes in the skin of mice. Furthermore, mice that were administered lycopene exhibited higher levels of translocation of nuclear-factor-erythroid-2-related factor 2 into the nucleus compared with the vehicle-treated and model mice. Collectively, these results indicated that lycopene exerts a protective effect against DMBA/TPA-induced cutaneum carcinoma through antioxidant defence.
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Phenolcarboxylic acids from medicinal herbs exert anticancer effects through disruption of COX-2 activity.
Phytomedicine
PUBLISHED: 04-06-2014
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Integrated research of herbs and formulas characterized by functions of promoting blood circulation and removing blood stasis is one of the most active fields in traditional Chinese medicine. This paper strives to demonstrate the roles of a homologous series of phenolcarboxylic acids from these medicinal herbs in cancer treatment via targeting cyclooxygenase-2 (COX-2), a well-recognized mediator in tumorigenesis. We selected thirteen typical phenolcarboxylic acids (benzoic acid derivatives, cinnamic acid derivatives and their dehydration-condensation products), and found gallic acid, caffeic acid, danshensu, rosmarinic acid and salvianolic acid B showed 50% inhibitory effects on hCOX-2 activity and A549 cells proliferation. 2D-quantitative method was introduced to describe the potential structural features that contributed to certain bioactivities. We also found these compounds underwent responsible hydrogen bonding to Arg120 and Ser353 in COX-2 active site residues. We further extensively focused on danshensu [d-(+)-?-(3,4-dihydoxy-phenylalanine)] or DSS, which exerted COX-2 dependent anticancer manner. Both genetic and pharmacological inhibition of COX-2 could enhance the ability of DSS inhibiting A549 cells growth. Additionally, COX-2/PGE2/ERK signaling axis was essential for the anticancer effect of DSS. Furthermore, combined treatment with DSS and celecoxib could produce stronger anticancer effects in experimental lung metastasis of A549 cells in vivo. All these findings indicated that phenolcarboxylic acids might possess anticancer effects through jointly targeting COX-2 activity in cancer cells and provided strong evidence in cancer prevention and therapy for the herbs characterized by blood-activating and stasis-resolving functions in clinic.
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The ERF transcription factor TaERF3 promotes tolerance to salt and drought stresses in wheat.
Plant Biotechnol. J.
PUBLISHED: 01-03-2014
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Salinity and drought are major limiting factors of wheat (Triticum aestivum) productivity worldwide. Here, we report the function of a wheat ERF transcription factor TaERF3 in salt and drought responses and the underlying mechanism of TaERF3 function. Upon treatment with 250 mM NaCl or 20% polyethylene glycol (PEG), transcript levels of TaERF3 were rapidly induced in wheat. Using wheat cultivar Yangmai 12 as the transformation recipient, four TaERF3-overexpressing transgenic lines were generated and functionally characterized. The seedlings of the TaERF3-overexpressing transgenic lines exhibited significantly enhanced tolerance to both salt and drought stresses as compared to untransformed wheat. In the leaves of TaERF3-overexpressing lines, accumulation levels of both proline and chlorophyll were significantly increased, whereas H?O? content and stomatal conductance were significantly reduced. Conversely, TaERF3-silencing wheat plants that were generated through virus-induced gene silencing method displayed more sensitivity to salt and drought stresses compared with the control plants. Real-time quantitative RT-PCR analyses showed that transcript levels of ten stress-related genes were increased in TaERF3-overexpressing lines, but compromised in TaERF3-silencing wheat plants. Electrophoretic mobility shift assays showed that the TaERF3 protein could interact with the GCC-box cis-element present in the promoters of seven TaERF3-activated stress-related genes. These results indicate that TaERF3 positively regulates wheat adaptation responses to salt and drought stresses through the activation of stress-related genes and that TaERF3 is an attractive engineering target in applied efforts to improve abiotic stress tolerances in wheat and other cereals.
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Epigenetic upregulation of corticotrophin-releasing hormone mediates postnatal maternal separation-induced memory deficiency.
PLoS ONE
PUBLISHED: 01-01-2014
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Accumulating evidences demonstrated that early postnatal maternal separation induced remarkable social and memory defects in the adult rodents. Early-life stress induced long-lasting functional adaptation of neuroendocrine hypothalamic-pituitary-adrenal axis, including neuropeptide corticotrophin-releasing hormone (CRH) in the brain. In the present study, a significantly increased hippocampal CRH was observed in the adult rats with postnatal maternal separation, and blockade of CRHR1 signaling significantly attenuated the hippocampal synaptic dysfunction and memory defects in the modeled rats. Postnatal maternal separation enduringly increased histone H3 acetylation and decreased cytosine methylation in Crh promoter region, resulting from the functional adaptation of several transcriptional factors, in the hippocampal CA1 of the modeled rats. Enriched environment reversed the epigenetic upregulation of CRH, and ameliorated the hippocampal synaptic dysfunction and memory defects in the adult rats with postnatal maternal separation. This study provided novel insights into the epigenetic mechanism underlying postnatal maternal separation-induced memory deficiency, and suggested environment enrichment as a potential approach for the treatment of this disorder.
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Dll4-Notch signaling in regulation of tumor angiogenesis.
J. Cancer Res. Clin. Oncol.
PUBLISHED: 08-19-2013
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Tumor angiogenesis is a complex process and involves the tight interplay of tumor cells, endothelial cells, phagocytes and their secreted factors, which may act as promoters or inhibitors of angiogenesis. Many signaling pathways involved in these processes such as vascular endothelial growth factor (VEGF), fibroblast growth factors, Wnt and mTOR signaling pathway. Though research has confirmed that VEGF can play an important role in tumor angiogenesis, and has designed a lot of drugs that target VEGF, both experimental and clinical studies showed that these pathways mentioned above including VEGF did not play key roles in tumor angiogenesis. With the deepening of the research, people find that of all the signaling pathways involved in tumor angiogenesis, Notch signaling is the most notable one and plays crucial role in tumor angiogenesis. It was previously recognized that the Notch signaling plays a key role only in physiological angiogenesis such as development, wound healing and pregnancy. However, an increasing number of studies have proved that Notch signaling is also involved in pathological angiogenesis such as tumor angiogenesis and plays a critical role in these processes. More importantly, compared to resistance caused by anti-VEGF or other signaling pathways, experimental evidence revealed that Notch was involved in anticancer drug resistance, indicating that targeting Notch could be a novel therapeutic approach to the treatment for cancer by overcoming drug resistance of cancer cells. More recently, research has demonstrated that Notch ligands Delta-like 4 (Dll4) plays a key role in tumor angiogenesis. Data show that Dll4 functions as a negative regulator of tumor angiogenesis and is upregulated in tumor vasculature. This review focus on recent insights into Dll4-Notch signaling in tumor angiogenesis and its mechanisms, which may be utilized for a potential pharmacological use as a target for anti-angiogenic cancer therapy.
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Saikosaponin D disrupts platelet-derived growth factor-? receptor/p38 pathway leading to mitochondrial apoptosis in human LO2 hepatocyte cells: a potential mechanism of hepatotoxicity.
Chem. Biol. Interact.
PUBLISHED: 05-03-2013
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Herbal hepatotoxicity has been increasingly reported in clinical context, but the underlying mechanisms are poorly understood. Saikosaponin D (SSD) is a major component of saikosaponins isolated from Bupleurum falactum, a herb that has been linked to hepatotoxicity. Our current study was to examine the toxic effect of SSD on human hepatocyte LO2 cells and explore the possible mechanism. The results demonstrated that SSD reduced cell viability and led to dramatic morphological alterations in LO2 cells. Hoechst staining and flow cytometry analyses showed that SSD stimulated hepatocyte apoptosis. SSD-treated cells exhibited apparent nuclear condensation and fragmentation, and the apoptotic cells were increased by SSD dose-dependently. Subsequent experiments showed that SSD decreased mitochondrial membrane potential and downregulated Bcl-2 but upregulated Bax. Moreover, caspase-9 and caspase-3 were activated in SSD-treated LO2 cells. These data consistently indicated that SSD stimulated mitochondrial apoptosis in hepatocytes. Mechanistic investigations showed that SSD disrupted p38 signaling and that p38 specific inhibitor SB203580 mimicked the pro-apoptotic effect of SSD. In addition, platelet-derived growth factor-? receptor (PDGF-?R) blocker imatinib reduced p38 phosphorylation and also mimicked the pro-apoptotic effect of SSD in LO2 cells. These data collectively indicated that SSD induced apoptosis by interrupting PDGF-?R/p38 pathway in LO2 hepatocytes.
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Expression of a potato antimicrobial peptide SN1 increases resistance to take-all pathogen Gaeumannomyces graminis var. tritici in transgenic wheat.
Funct. Integr. Genomics
PUBLISHED: 03-03-2013
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Take-all, caused by soil-borne fungus Gaeumannomyces graminis var. tritici (Ggt), is a devastating root disease of wheat (Triticum aestivum) worldwide. Breeding resistant wheat cultivars is the most promising and reliable approach to protect wheat from take-all. Currently, no resistant wheat germplasm is available to breed cultivars using traditional methods. In this study, gene transformation was carried out using Snakin-1 (SN1) gene isolated from potato (Solanum tuberosum) because the peptide shows broad-spectrum antimicrobial activity in vitro. Purified SN1 peptide also inhibits in vitro the growth of Ggt mycelia. By bombardment-mediated method, the gene SN1 was transformed into Chinese wheat cultivar Yangmai 18 to generate SN1 transgenic wheat lines, which were used to assess the effectiveness of the SN1 peptide in protecting wheat from Ggt. Genomic PCR and Southern blot analyses indicated that the alien gene SN1 was integrated into the genomes of five transgenic wheat lines and heritable from T? to T? progeny. Reverse transcription-PCR and Western blot analyses showed that the introduced SN1 gene was transcribed and highly expressed in the five transgenic wheat lines. Following challenging with Ggt, disease test results showed that compared to segregants lacking the transgene and untransformed wheat plants, these five transgenic wheat lines expressing SN1 displayed significantly enhanced resistance to take-all. These results suggest that SN1 may be a potentially transgenic tool for improving the take-all resistance of wheat.
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Holothurian glycosaminoglycan inhibits metastasis and thrombosis via targeting of nuclear factor-?B/tissue factor/Factor Xa pathway in melanoma B16F10 cells.
PLoS ONE
PUBLISHED: 01-10-2013
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Holothurian glycosaminoglycan (hGAG) is a high-molecular-weight form of fucosylated chondroitin sulfate and has an antithrombotic effect. Our previous studies demonstrated that hGAG efficiently inhibited tumor cell metastasis. The interplays between thrombosis and tumor progression may have a major impact on hematogenous metastasis. In this study, we demonstrated that the mouse melanoma B16F10 cells treated with hGAG displayed a significant reduction of metastasis and coagulation capacity in vitro and in vivo. Mechanistic studies revealed that hGAG treatment in B16F10 cells remarkably inhibited the formation of fibrin through attenuating the generation of activated Factor Xa (FXa), without affecting the expression of urokinase (uPA) and plasminogen activator inhibitor 1 (PAI-1) that involved in fibrinolysis. Moreover, hGAG treatment downregulated the transcription and protein expression of tissue factor (TF). Promoter deletions, site mutations and functional studies identified that the nuclear transcription factor NF-?B binding region is responsible for hGAG-induced inhibition of TF expression. While the hGAG treatment of B16F10 cells was unable to inhibit NF-?B expression and phosphorylation, hGAG significantly prevented nuclear translocation of NF-?B from the cytosol, a potential mechanism underlying the transcriptional suppression of TF. Moreover, hGAG markedly suppressed the activation of p38MAPK and ERK1/2 signaling pathways, the central regulators for the expression of metastasis-related matrix metalloproteinases (MMPs). Consequently, hGAG exerts a dual function in the inhibition of metastasis and coagulation activity in mouse melanoma B16F10 cells. Our studies suggest hGAG to be a promising therapeutic agent for metastatic cancer treatment.
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Inhibition of vascular endothelial growth factor-mediated angiogenesis involved in reproductive toxicity induced by sesquiterpenoids of Curcuma zedoaria in rats.
Reprod. Toxicol.
PUBLISHED: 01-09-2013
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The use of herbal medicine has rapidly increased in recent decades, prompting an increase in toxicity concerns. Here we investigated whether and how essential oil of Curcuma zedoaria may induce reproductive and developmental toxicity. Whole embryo culture in rats revealed that the essential oil produced a concentration-dependent toxicity ex vivo in the embryos on gestation Day 9.5 (GD9.5). Weight loss, abnormal hematological and biochemical effects on dams and embryos were also observed in GD17 pregnant rats orally administrated with 100mgkg(-1) or 200mgkg(-1) essential oil from GD7 onward. Induction of embryotoxicity may be related to placental calcification attributed to inhibition of vascular endothelial growth factor (VEGF)-mediated angiogenesis. Analysis by gas chromatography-mass spectrometry demonstrated that the main toxic compounds in essential oil were sesquiterpenoids. Our results suggest that the reproductive toxicity of C. zedoaria may be caused by sesquiterpenoids in the essential oil blocking VEGF-mediated angiogenesis.
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Concerted Suppression of STAT3 and GSK3? Is Involved in Growth Inhibition of Non-Small Cell Lung Cancer by Xanthatin.
PLoS ONE
PUBLISHED: 01-01-2013
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Xanthatin, a sesquiterpene lactone purified from Xanthium strumarium L., possesses prominent anticancer activity. We found that disruption of GSK3? activity was essential for xanthatin to exert its anticancer properties in non-small cell lung cancer (NSCLC), concurrent with preferable suppression of constitutive activation of STAT3. Interestingly, inactivation of the two signals are two mutually exclusive events in xanthatin-induced cell death. Moreover, we surprisingly found that exposure of xanthatin failed to trigger the presumable side effect of canonical Wnt/?-Catenin followed by GSK3? inactivation. We further observed that the downregulation of STAT3 was required for xanthatin to fine-tune the risk. Thus, the discovery of xanthatin, which has ability to simultaneously orchestrate two independent signaling cascades, may have important implications for screening promising drugs in cancer therapies.
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Natural history of prenatal ventricular septal defects and their association with foetal echocardiographic features.
Cardiol Young
PUBLISHED: 11-04-2011
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To describe the evolution of ventricular septal defects in infants from intra-uterine diagnosis to the age of 3 years or until documented echocardiographic closure of the defect, as well as any relationship between closure rate, time and foetal echocardiographic features.
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Anti-angiogenesis effect of essential oil from Curcuma zedoaria in vitro and in vivo.
J Ethnopharmacol
PUBLISHED: 07-19-2011
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Curcuma zedoaria (Berg.) Rosc., a traditional Chinese herb, was used widely but absolutely prohibited for the pregnant in clinic. Based on that there is abundant angiogenesis in endometrium and placenta during gestation period, we hypothesized that some components from it could inhibit angiogenesis and then damaged the supply of oxygen and nutrition to the embryo, which finally led to gestation failure.
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[Determination of plasma concentration of pachyman sulfate by spectrophotometry and its pharmacokinetics after intraperitoneal and intravenous administrations in rats].
Zhongguo Zhong Yao Za Zhi
PUBLISHED: 09-27-2010
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To develop a spectral assay for determination of pachyman sulfate (PS) in rat plasma and to study the pharmacokinetics after intraperitoneal and intravenous administrations of PS.
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Beta-elemene inhibits melanoma growth and metastasis via suppressing vascular endothelial growth factor-mediated angiogenesis.
Cancer Chemother. Pharmacol.
PUBLISHED: 03-21-2010
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It was to assess antiangiogenic effect of ?-elemene in vitro and in vivo, and it was involved in inhibiting melanoma growth and metastasis, as well as to elucidate its intrinsic mechanism.
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Acidic mucopolysaccharide from Holothuria leucospilota has antitumor effect by inhibiting angiogenesis and tumor cell invasion in vivo and in vitro.
Cancer Biol. Ther.
PUBLISHED: 08-08-2009
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Acidic mucopolysaccharide from Holothuria Leucospilota (HS) may affect some steps in metastasis cascade. In vitro, HS inhibited the growth of B16F10 cells and proliferation of VEGF-induced HUVEC dose-dependently compared to the control, VEGF-induced capillary-like tube networks and the numbers of migratory and invasive cells were significantly inhibited by HS in a dose-dependent manner under the cytotoxic doses. Additionally, VEGF-induced vessel sprouting of rat aortic ring was also inhibited by HS. It also has been demonstrated that the invasive ability of B16F10 melanoma cells through the Matrigel-embedded Boyden chamber was suppressed by 0.5 muM HS. The protein level secreted by B16F10 cells of MMP-2,-9 and VEGF were decreased by HS treatment. In vivo, a tumor growth inhibition study was carried out using mice bearing B16F10 cells model of metastasis, no matter experimental or spontaneous, showed that HS at 5.2, 11.6 and 26 mg/kg (weight of mice) could markedly decreased the metastatic tumors in mouse lung in a dose-dependent manner. In CAM assay and Matrigel plug assay in vivo, HS (50 microg/egg and 100 microg/egg) inhibited new blood vessel formation on the growing chick chorioallantoic membrane, and HS (5.2 and 26 mg/kg body weight) reduced the vessel density in Matrigel plugs implanted in mice. Taken together, these results demonstrate that HS has antimetastasic properties possibly via its antiangiogenesis induced by downregulation of VEGF and suppression of invasive ability of cancer cells mediated by downregulation of MMP-2, -9 and their activities.
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[Effect of danshensu on redox state and relevant nuclear transcription factors in non-small cell lung cancer A549 cells].
Zhongguo Zhong Yao Za Zhi
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To study the molecular mechanism of anti-tumor effect of Danshensu (DSS) focusing on whether it is related to its antioxidation effect on redox state of non-small cell lung cancer A549 cells and relevant nuclear transcription factors and signal pathway.
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[Plasma metabonomics study of ischemic cerebral apoplexy rats treated with Tongsaimai pellets].
Zhongguo Zhong Yao Za Zhi
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To observe abnormal metabolic changes caused by ischemic cerebral apoplexy and the regulating action of Tongsaimai pellets on abnormal metabolism by analyzing the change of small molecules in plasma of ischemic cerebral apoplexy rat. To find the potential biomarkers, and to explore metabolic mechanisms of Tongsaimai pellets.
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Xanthatin induces G2/M cell cycle arrest and apoptosis in human gastric carcinoma MKN-45 cells.
Planta Med.
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Xanthatin, a natural bioactive compound of sesquiterpene lactones, was isolated and purified from air-dried aerial part of Xanthium sibiricum Patrin ex Widder. In the present study, we demonstrated the significant antiproliferative and proapoptotic effects of xanthatin on human gastric carcinoma MKN-45 cells. MTS assay showed that xanthatin produced obvious cytotoxicity in MKN-45 cells with IC50 values of 18.6, 9.3, and 3.9 ┬ÁM for 12, 24, and 48 h, respectively. Results of flow cytometry analysis indicated that the antiproliferative activity induced by xanthatin might be executed via G2/M cell cycle arrest and proapoptosis in MKN-45 cells. Western blot analysis elucidated that: a) xanthatin downregulated expression of Chk1 and Chk2 and phosphorylation of CDC2, which are known as key G2/M transition regulators; b) xanthatin increased p53 activation, decreased the bcl-2/bax ratio and the levels of downstream procaspase-9 and procaspase-3, which are key regulators in the intrinsic apoptosis pathway; c) xanthatin blocked phosphorylation of NF-?B (p65 subunit) and of I?B?, which might contribute to its proapoptotic effects on MKN-45 cells. In conclusion, our results suggest that xanthatin may have therapeutic potential against human gastric carcinoma.
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Xanthatin induces cell cycle arrest at G2/M checkpoint and apoptosis via disrupting NF-?B pathway in A549 non-small-cell lung cancer cells.
Molecules
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Xanthatin, a natural sesquiterpene lactone, has significant antitumor activity against a variety of cancer cells, yet little is known about its anticancer mechanism. In this study, we demonstrated that xanthatin had obvious dose-/time-dependent cytotoxicity against the human non-small-cell lung cancer (NSCLC) cell line A549. Flow cytometry analysis showed xanthatin induced cell cycle arrest at G2/M phase. Xanthatin also had pro-apoptotic effects on A549 cells as evidenced by Hoechst 33258 staining and annexin V-FITC staining. Mechanistic data revealed that xanthatin downregulated Chk1, Chk2, and phosphorylation of CDC2, which contributed to the cell cycle arrest. Xathatin also increased total p53 protein levels, decreased Bcl-2/Bax ratio and expression of the downstream factors procaspase-9 and procaspase-3, which triggered the intrinsic apoptosis pathway. Furthermore, xanthatin blocked phosphorylation of NF-?B (p65) and I?Ba, which might also contribute to its pro-apoptotic effects on A549 cells. Xanthatin also inhibited TNFa induced NF-?B (p65) translocation. We conclude that xanthatin displays significant antitumor effects through cell cycle arrest and apoptosis induction in A549 cells. These effects were associated with intrinsic apoptosis pathway and disrupted NF-?B signaling. These results suggested that xanthatin may have therapeutic potential against NSCLC.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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