Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association最新文献

A protective role of heme-regulated eIF2α kinase in cadmium-induced toxicity in erythroid cells. 血红素调控的eIF2α激酶在镉致红细胞毒性中的保护作用。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-22 DOI: 10.1016/j.fct.2013.10.017

Lixin Wang, Xiaoyan Wang, Shuping Zhang, Guangbo Qu, Sijin Liu

{"title":"A protective role of heme-regulated eIF2α kinase in cadmium-induced toxicity in erythroid cells.","authors":"Lixin Wang, Xiaoyan Wang, Shuping Zhang, Guangbo Qu, Sijin Liu","doi":"10.1016/j.fct.2013.10.017","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.017","url":null,"abstract":"Although a number of studies have demonstrated that cadmium (Cd) can incur damage to mature red cells, the potential injuries of Cd to erythroid progenitor cells have not been investigated thus far. Heme-regulated eIF2α kinase (Hri) is essential for translational regulation and survival of erythroid precursors in the setting of iron deficiency. Hri has been demonstrated to activate Atf4 signaling in reducing oxidative stress and in promoting erythroid differentiation during stress erythropoiesis. Here, we demonstrated that Cd significantly provoked cell death and suppressed erythroid differentiation of erythroid progenitor cells. Importantly, our results established a crucial role of Hri in ameliorating Cd-induced impairment to erythropoiesis. Upon Cd treatment, Hri-eIF2αP-Atf4 signaling was activated to protect cells from cell death and differentiation attenuation in Wt fetal liver erythroblasts; in contrast, Hri(-/-) erythroblasts suffered from enhanced oxidative stress, as evidenced by increased levels of reactive oxygen species (ROS) and consequentially elevated apoptosis. As for Cd administration in vivo, impaired erythropoiesis in bone marrow and dramatic extramedullary erythropoiesis in spleen were observed in Hri(-/-) mice. Taken together, our combined data highlighted a crucial role of Hri in protecting survival and differentiation of erythroid progenitor cells upon Cd treatment. ","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"880-91"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40267682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

5,6,7-trimethoxyflavone suppresses pro-inflammatory mediators in lipopolysaccharide-induced RAW 264.7 macrophages and protects mice from lethal endotoxin shock. 5,6,7-三甲氧基黄酮抑制脂多糖诱导的RAW 264.7巨噬细胞的促炎介质，并保护小鼠免受致死性内毒素休克。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-24 DOI: 10.1016/j.fct.2013.10.025

Hong-Kun Rim, Chang Hyeon Yun, Ji-Sun Shin, Young-Wuk Cho, Dae Sik Jang, Jong Hoon Ryu, Haeil Park, Kyung-Tae Lee

{"title":"5,6,7-trimethoxyflavone suppresses pro-inflammatory mediators in lipopolysaccharide-induced RAW 264.7 macrophages and protects mice from lethal endotoxin shock.","authors":"Hong-Kun Rim, Chang Hyeon Yun, Ji-Sun Shin, Young-Wuk Cho, Dae Sik Jang, Jong Hoon Ryu, Haeil Park, Kyung-Tae Lee","doi":"10.1016/j.fct.2013.10.025","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.025","url":null,"abstract":"5,6,7-Trimethoxyflavone (TMF), methylations of the hydroxyl groups of oroxylin A or baicalein, was found to significantly inhibit the productions of nitric oxide (NO) and prostaglandin E2 (PGE2) in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. However, no report has been issued on the anti-inflammatory potential of TMF and the underlying molecular mechanism. In the present study, we investigated the anti-inflammatory effects of TMF in LPS-induced RAW 264.7 macrophages and LPS-induced septic shock in mice. TMF dose-dependently inhibits iNOS and COX-2 at the protein, mRNA, and promoter binding levels and that these inhibitions cause attendant decreases in the productions of NO and PGE2. TMF inhibits the productions and mRNA expressions of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 induced by LPS. Furthermore, TMF suppress the transcriptional activity of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1), and nuclear translocations of NF-κB, AP-1, and signal transducer and activator of transcription 1/3 (STAT1/3). Pretreatment with TMF increase the survival rate of mice with LPS-induced endotoxemia and reduced the serum levels of cytokines. Taken together, these findings suggest that TMF down-regulates the expressions of the pro-inflammatory iNOS, COX-2, TNF-α, IL-1β, and IL-6 genes in macrophages by interfering with the activation of NF-κB, AP-1, and STAT1/3. ","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"847-55"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40266463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14

Extra virgin olive oil potentiates the effects of aromatase inhibitors via glutathione depletion in estrogen receptor-positive human breast cancer (MCF-7) cells. 特级初榨橄榄油通过谷胱甘肽耗损雌激素受体阳性人乳腺癌(MCF-7)细胞增强芳香酶抑制剂的作用。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-23 DOI: 10.1016/j.fct.2013.10.024

Amar Mohamed Ismail, Lionel L A In, Mohammad Tasyriq, Devi Rosmy Syamsir, Khalijah Awang, Ayda Hussein Omer Mustafa, Omer Fadul Idris, Imad Fadl-Elmula, Noor Hasima

{"title":"Extra virgin olive oil potentiates the effects of aromatase inhibitors via glutathione depletion in estrogen receptor-positive human breast cancer (MCF-7) cells.","authors":"Amar Mohamed Ismail, Lionel L A In, Mohammad Tasyriq, Devi Rosmy Syamsir, Khalijah Awang, Ayda Hussein Omer Mustafa, Omer Fadul Idris, Imad Fadl-Elmula, Noor Hasima","doi":"10.1016/j.fct.2013.10.024","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.024","url":null,"abstract":"There have been numerous evidences supporting the relationship between olive oil and cancer, with most of the attention being directed toward its fat and phenolic content. The aims of this study were to investigate whether EVOO and OA could enhance the effects of aromatase inhibitors (letrozole and anastrozole) in ER-positive MCF-7 cells, as well as to investigate its influence on cytochrome c release and GSH levels. It was observed that upon combination treatment, anti-proliferation effects and apoptosis induction were augmented. Apoptosis was triggered via the intrinsic pathway in accordance with cytochrome c release into the cytosol based on IF-IC and ELISA observations. Intracellular GSH levels were also reduced upon EVOO/OA treatment in combination with aromatase inhibitors, and were found to be inversely correlated to cytosolic cytochrome c levels. Additionally, the estrogenic suppressive effects of letrozole and anastrozole were amplified when used in combination with EVOO/OA. Therefore, the employment of aromatase inhibitors in combination with EVOO/OA could orchestrate a reduction in intracellular estrone biosynthesis which feeds ER-positive cells, while simultaneously depleting GSH levels and increasing ROS generation, thus releasing cytochrome c and subsequent induction of apoptosis in MCF-7 cells. ","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"817-24"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40266466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

Galangin inhibits proliferation of hepatocellular carcinoma cells by inducing endoplasmic reticulum stress. 高良姜通过诱导内质网应激抑制肝癌细胞增殖。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-22 DOI: 10.1016/j.fct.2013.10.019

Lijuan Su, Xiaoyi Chen, Jun Wu, Biyun Lin, Haitao Zhang, Liubo Lan, Hui Luo

{"title":"Galangin inhibits proliferation of hepatocellular carcinoma cells by inducing endoplasmic reticulum stress.","authors":"Lijuan Su, Xiaoyi Chen, Jun Wu, Biyun Lin, Haitao Zhang, Liubo Lan, Hui Luo","doi":"10.1016/j.fct.2013.10.019","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.019","url":null,"abstract":"Prolonged endoplasmic reticulum (ER) stress may activate apoptotic pathways in cancer cells. It is suggested that ER stress has the potential of enhancing tumor death in cancer therapy. Galangin, a flavonol derived from Alpinia officinarum Hance, has been shown to suppress the proliferation of hepatocellular carcinoma cells (HCC). The aim of this study was to determine whether galangin was able to induce ER stress in HepG2, Hep3B and PLC/PRF/5 cells. The proliferation of HCC was tested by MTT method. Intracellular Ca(2+) levels were measured with Fluo3-AM.The proteins levels of GRP94, GRP78 and CHOP were detected by Western blot. To further understand the anti-HCC mechanism of galangin, mitogen-activated protein kinases (MAPKs) were detected. The results showed that galangin treatment induced ER stress was evidenced by increased protein levels of GRP94, GRP78 and CHOP, as well as increased free cytosolic Ca(2+) concentration. ER stress inhibitor 4-PBA and CHOP siRNA blocked significantly galangin-induced ER in all three cell lines. Further experiments showed that MAPKs involved in ER stress induced by galangin. In summary, galangin is identified as a stimulator of ER stress to suppress the proliferation of HCC, and may be used as a potential anti-cancer agent.","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"810-6"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40267680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 60

TNFR1/TNF-α and mitochondria interrelated signaling pathway mediates quinocetone-induced apoptosis in HepG2 cells. TNFR1/TNF-α和线粒体相关信号通路介导喹诺酮诱导的HepG2细胞凋亡。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-22 DOI: 10.1016/j.fct.2013.10.022

Chaoming Zhang, Congcong Wang, Shusheng Tang, Yu Sun, Dongxu Zhao, Shen Zhang, Sijun Deng, Yan Zhou, Xilong Xiao

{"title":"TNFR1/TNF-α and mitochondria interrelated signaling pathway mediates quinocetone-induced apoptosis in HepG2 cells.","authors":"Chaoming Zhang, Congcong Wang, Shusheng Tang, Yu Sun, Dongxu Zhao, Shen Zhang, Sijun Deng, Yan Zhou, Xilong Xiao","doi":"10.1016/j.fct.2013.10.022","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.022","url":null,"abstract":"Quinocetone, a new quinoxaline 1, 4-dioxide derivative, has been widely used as an animal feed additive in China. This study was conducted to explore the molecular mechanisms of apoptosis induced by quinocetone in HepG2 cells. MTT assay revealed that the viability of HepG2 cells was significantly inhibited by quinocetone in a dose- and time-dependent manner. Quinocetone-induced apoptosis in HepG2 cells was characterized by cell and nuclei morphology change, cell membrane phosphatidylserine translocation, DNA fragmentation, cleavage of poly (ADP-ribose) polymerase (PARP) and a cascade activation of caspase-8, caspase-9 and caspase-3. Simultaneously, quinocetone induced HepG2 cell cycle arrest, which was supported by overexpression of p21. Cytochrome c release was caused by the mitochondrial membrane potential dissipation, a process related to quinocetone-induced Bid cleavage and elevated Bax/Bcl-2 ratio. Moreover, quinocetone treatment caused the up-regulation of TNF-α and TNFR1 in HepG2 cells. Both soluble TNFR1 receptors and caspase inhibitors suppressed quinocetone-induced apoptosis. In addition, the protein levels of p53, p-p38 and p-JNK were increased in quinocetone-treated cells. Taken together, quinocetone induced apoptosis in HepG2 cells via activation of caspase, interaction of TNF-α and TNFR1 and modulation of the protein levels of Bid, Bax and Bcl-2, involving the participation of p53, p38 and JNK. ","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"825-38"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40267681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 42

Astaxanthin and omega-3 fatty acids individually and in combination protect against oxidative stress via the Nrf2-ARE pathway. 虾青素和omega-3脂肪酸单独或联合通过Nrf2-ARE途径防止氧化应激。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-21 DOI: 10.1016/j.fct.2013.10.023

Constance Lay Lay Saw, Anne Yuqing Yang, Yue Guo, Ah-Ng Tony Kong

{"title":"Astaxanthin and omega-3 fatty acids individually and in combination protect against oxidative stress via the Nrf2-ARE pathway.","authors":"Constance Lay Lay Saw, Anne Yuqing Yang, Yue Guo, Ah-Ng Tony Kong","doi":"10.1016/j.fct.2013.10.023","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.023","url":null,"abstract":"Oxidative stress is a major driver of many diseases, including cancer. The induction of Nrf2-ARE-mediated antioxidant enzymes provides a cellular defense against oxidative stress. Astaxanthin (AST), a red dietary carotenoid, possesses potent antioxidant activity, and inhibits oxidative damages. Polyunsaturated fatty acids (PUFAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are important nutritional essentials and potent antioxidants found in fish oil. In the present study, we investigated whether AST in combination with low concentrations of DHA or EPA has a synergistic antioxidant effect in a HepG2-C8-ARE-luciferase cell line system. Using free radical scavenging DPPH assay, AST was more potent DPPH radical scavenger than DHA and EPA. MTS assay revealed that AST was non-toxic up to 100μM compared with more toxic DHA and EPA. The three compounds alone and in combination elevated cellular GSH levels, increased the total antioxidant activity, induced mRNA expression of Nrf2 and Nrf2 downstream target genes NQO1, HO-1, and GSTM2. Lower concentrations of AST show synergistic effects when combined with DHA or EPA. In summary, our study shows synergistic antioxidant effects of AST and PUFAs at low concentrations. The Nrf2/ARE pathway plays an important role in the antioxidative effects induced by AST, DHA, and EPA. ","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"869-75"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40264171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 126

Effects of red ginseng on the regulation of cyclooxygenase-2 of spleen cells in whole-body gamma irradiated mice. 红参对γ辐照小鼠脾脏细胞环氧化酶-2的调节作用。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-24 DOI: 10.1016/j.fct.2013.10.009

Hyun Jung Koo, Seon-A Jang, Kwang-Hee Yang, Se Chan Kang, Seung Namkoong, Tae-Hyung Kim, Do Thi Thu Hang, Eun-Hwa Sohn

{"title":"Effects of red ginseng on the regulation of cyclooxygenase-2 of spleen cells in whole-body gamma irradiated mice.","authors":"Hyun Jung Koo, Seon-A Jang, Kwang-Hee Yang, Se Chan Kang, Seung Namkoong, Tae-Hyung Kim, Do Thi Thu Hang, Eun-Hwa Sohn","doi":"10.1016/j.fct.2013.10.009","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.009","url":null,"abstract":"Exposure to gamma radiation causes a wide range of biological damage and alterations, including oxidative stress, inflammation and cancer. This study aimed to identify the radioprotective effect of Korean red ginseng extract (RG) against whole-body gamma-irradiation (γIR) in mice and the regulatory mechanisms of the radiosensitive gene in spleen, cyclooxygenase-2 (COX-2). RG was administered intraperitoneally (i.p.) or orally (p.o.) to C57BL/6 mice for five days, which were then exposed to 6.5 Gy of (137)Cs-γIR. Thymus and spleen were harvested after three days, and organ size and COX-2 expression of the spleen using Western blotting, were examined. γIR shrank both organs and RG recovered the size of thymus but not spleen. RG also significantly inhibited the increased expression of COX-2 induced by γIR. These results were similar following both routes of RG administration, however i.p. RG administration was more effective, thus it was used in progressive studies. In terms of COX-2 expression related intracellular factors, we found here that γIR activated the p38 MAPK, PI3K/Akt and HO-1 but not NF-κB or Nrf2. Activated p38 MAPK, PI3K/Akt and HO-1 were down-regulated by RG while the RG-induced COX-2 expression was only related to HO-1 activation. These results suggest that RG supplementation provides protective effects against radiation-induced inflammation and cancer, and its potential to be utilized in clinical trials and functional foods.","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"839-46"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40266464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17

Rubus idaeus L. reverses epithelial-to-mesenchymal transition and suppresses cell invasion and protease activities by targeting ERK1/2 and FAK pathways in human lung cancer cells. Rubus idaeus L.通过靶向ERK1/2和FAK通路，逆转人肺癌细胞上皮向间质转化，抑制细胞侵袭和蛋白酶活性。

IF 4.3

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Pub Date : 2013-12-01 Epub Date: 2013-10-24 DOI: 10.1016/j.fct.2013.10.021

Yih-Shou Hsieh, Shu-Chen Chu, Li-Sung Hsu, Kuo-Shuen Chen, Ming-Tsung Lai, Chia-Heng Yeh, Pei-Ni Chen

{"title":"Rubus idaeus L. reverses epithelial-to-mesenchymal transition and suppresses cell invasion and protease activities by targeting ERK1/2 and FAK pathways in human lung cancer cells.","authors":"Yih-Shou Hsieh, Shu-Chen Chu, Li-Sung Hsu, Kuo-Shuen Chen, Ming-Tsung Lai, Chia-Heng Yeh, Pei-Ni Chen","doi":"10.1016/j.fct.2013.10.021","DOIUrl":"https://doi.org/10.1016/j.fct.2013.10.021","url":null,"abstract":"Epithelial to mesenchymal transition (EMT) has been considered essential for cancer metastasis, a multistep complicated process including local invasion, intravasation, extravasation, and proliferation at distant sites. Herein we provided molecular evidence associated with the antimetastatic effect of Rubus idaeus L. extracts (RIE) by showing a nearly complete inhibition on the invasion (p<0.001) of highly metastatic A549 cells via reduced activities of matrix metalloproteinase-2 (MMP-2) and urokinasetype plasminogen activator (u-PA). We performed Western blot to find that RIE could induce up-regulation of epithelial marker such as E-cadherin and α-catenin and inhibit the mesenchymal markers such as N-cadherin, fibronectin, snail-1, and vimentin. Selective snail-1 inhibition by snail-1-specific-siRNA also showed increased E-cadherin expression in A549 cells suggesting a possible involvement of snail-1 inhibition in RIE-caused increase in E-cadherin level. RIE also inhibited p-FAK, p-paxillin and AP-1 by Western blot analysis, indicating the anti-EMT effect of RIE in human lung carcinoma. Importantly, an in vivo BALB/c nude mice xenograft model showed that RIE treatment reduced tumor growth by oral gavage, and RIE represent promising candidates for future phytochemical-based mechanistic pathway-targeted cancer prevention strategies. ","PeriodicalId":510137,"journal":{"name":"Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association","volume":" ","pages":"908-18"},"PeriodicalIF":4.3,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.fct.2013.10.021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40266465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 51