Abstract:Objecitve: Ochratoxin A (OTA) is a naturally occurring mycotoxin, our previous study demonstrated that OTA evoked cell cycle arrest at G2 phase in GES-1 cells. The aim of the present study was to explore the putative role of p38 MAPK signaling pathway in OTA-induced G2 phase arrest in human gastric epithelium cells (GES-1) in vitro. Methods: After treated with different concentrations of OTA (0, 5, 10 and 20 μM) for 24 h, the expression of p38/Phospho-p38 at protein level in GES-1 cells was determined by Western blot. GES-1 cells were then preincubated with SB203580 (10 μM) for 30 min or reversely transfected with siRNA targeting p38, then the distribution of cell cycle phases was detected by Flow cytometry, and the expression of Cdc25C/p-Cdc25C, Cdc2/p-Cdc2, CyclinB1 and complex of Cdc2-CyclinB1 were detected by Western blot analysis and Immunoprecipitation. Results: OTA at different concentrations of 5, 10 and 20 μM for 24 h could activate p38 MAPK signaling pathway of GES-1 cells. p38 specific inhibitor (SB203580) and p38 siRNA transfaction blocked the down-regulation of Cdc25C/p-Cdc25C, Cdc2/p-Cdc2, CyclinB1 and complex of Cdc2-CyclinB1, and then abolished the G2 arrest induced by OTA. Conclusion: p38 MAPK signaling pathway was involved in OTA-induced G2 arrest in GES-1 cells by modulating G2 phase related factors.

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	1. Ochratoxin A-induced G2 phase arrest in human gastric epithelium cells via p38 MAPK signaling pathway
	WANG Yuan,LIU Jing,CUI Jinfeng,XING Lingxiao,WANG Junling,YAN Xia,ZHANG Xianghong
	Basic Medicine 05 August 2012
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	Abstract:Objecitve: Ochratoxin A (OTA) is a naturally occurring mycotoxin, our previous study demonstrated that OTA evoked cell cycle arrest at G2 phase in GES-1 cells. The aim of the present study was to explore the putative role of p38 MAPK signaling pathway in OTA-induced G2 phase arrest in human gastric epithelium cells (GES-1) in vitro. Methods: After treated with different concentrations of OTA (0, 5, 10 and 20 μM) for 24 h, the expression of p38/Phospho-p38 at protein level in GES-1 cells was determined by Western blot. GES-1 cells were then preincubated with SB203580 (10 μM) for 30 min or reversely transfected with siRNA targeting p38, then the distribution of cell cycle phases was detected by Flow cytometry, and the expression of Cdc25C/p-Cdc25C, Cdc2/p-Cdc2, CyclinB1 and complex of Cdc2-CyclinB1 were detected by Western blot analysis and Immunoprecipitation. Results: OTA at different concentrations of 5, 10 and 20 μM for 24 h could activate p38 MAPK signaling pathway of GES-1 cells. p38 specific inhibitor (SB203580) and p38 siRNA transfaction blocked the down-regulation of Cdc25C/p-Cdc25C, Cdc2/p-Cdc2, CyclinB1 and complex of Cdc2-CyclinB1, and then abolished the G2 arrest induced by OTA. Conclusion: p38 MAPK signaling pathway was involved in OTA-induced G2 arrest in GES-1 cells by modulating G2 phase related factors.
	TO cite this article:WANG Yuan,LIU Jing,CUI Jinfeng, et al. Ochratoxin A-induced G2 phase arrest in human gastric epithelium cells via p38 MAPK signaling pathway[OL].[ 5 August 2012] http://en.paper.edu.cn/en_releasepaper/content/4486367


	2. Expression of calponin h2 in anti-Thy-1.1 nephritis: negative correlation with TGF beta1 expression
	LI Hui
	Basic Medicine 08 February 2012
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	Abstract:BACKGROUND: Evidence implied that calponin h2 (CNh2), an actin-binding protein, may be an antiproliferative gene. However, the expression of CNh2 in anti Thy1.1 glomerulonephritis (ATG) has not yet become clear. In this study, we sought to assess the relationship between CNh2 and transforming growth factor beta 1(TGF-β1) expression in vitro and in vivo. METHODS: In vivo study, ATG rats were generated and expression of CNh2 and TGF-β1 were assessed by immunohistochemistry, reverse transcription polymerase chain reaction (RT-PCR) and western blot, respectively. In vitro study, cultured mesangial cells(MsC) were stimulated with 2.08mmol/L argrinine or 200mmol/L ethanol for 48 hour, then expression of CNh2 and TGF-β1 were evaluated at the mRNA and protein level. RESULTS: CNh2 expression enhanced from day 3 to day 14, whereas TGF-β1 expression greatly increased from day 7 to day 28 in ATG (P<0.05). Up-regulation of TGF-β1expression and down-regulation of CNh2 expression were observed in MsC incubated with argrinine, whereas increased TGF-β1 expression and decreased CNh2 expression were shown in MsC treated with ethanol. CONCLUSIONS: CNh2 expression was enhanced in the early stage of ATG. With the progression of ATG, CNh2 expression decreased accompanied by an evident increase in TGF-β1 expression. CNh2 may function as a negative feedback regulator of TGF-β1 expression in rat MsC.
	TO cite this article:LI Hui. Expression of calponin h2 in anti-Thy-1.1 nephritis: negative correlation with TGF beta1 expression[OL].[ 8 February 2012] http://en.paper.edu.cn/en_releasepaper/content/4465455

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	3. VEGF is involved in the increase of dermal microvessel permeability induced by tryptase
	Bai Qianming,Wang Xinhong,Xu Yali,Yin Lianhua,Li Xiaobo
	Basic Medicine 31 January 2012
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	Abstract:Mast cells abundantly reside near the dermal vessels and release tryptase in the condition of cutaneous hypersensitivity and allergy, which is meanifested by rapid edema due to increased vascular permeability. However, the mechanism of mast cell tryptase promoting permeability remains to be defined. In this study, we investigated the effect of tryptase/human mast cells (HMC-1) supernatant on the permeability of human dermal microvascular endothelial cells (HDMECs) and studied whether vascular endothelial growth factor (VEGF) is involved in this effect or not. HMC-1 cells released tryptase pro-degranulating agent a23187 dose-dependently and HMC-1 cells density-dependently. Both tryptase and HMC-1 supernatant can promote permeability of HDMECs dramatically dose-dependently, which was resisted by tryptase inhibitor APC366 (a specific tryptase inhibitor) and partially reversed by a VEGF neutralizing antibody. Tryptase added to HDMECs caused a significant increase of mRNA and protein levels of VEGF, VEGF receptors (Flt-1 and Flk-1) by Real-time RT-PCR assay and Western-blot respectively. Our results suggest that mast cells tryptase can up-regulate the expression of VEGF and VEGF receptors. The VEGF neutralizing antibody can block the dermal microvessel hypermeability induced by tryptase. Thus, VEGF is involved in the increase of tryptse-induced dermal microvessel hypermeability and edema.
	TO cite this article:Bai Qianming,Wang Xinhong,Xu Yali, et al. VEGF is involved in the increase of dermal microvessel permeability induced by tryptase[OL].[31 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4464501


	4. TEIF associated centrosomal activity is regulated by EGF/PI3K/Akt signaling
	ZHAO Jing,CHI Yingkai,LIU Haijing,ZOU Yongxin,CUI Suping,JIANG Ping,WANG Huali,ZHANG Hong,MAO Jingzhuo,HOU Lin,ZHANG Bo
	Basic Medicine 11 January 2012
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	Abstract:Centrosome amplification, a characteristic of cancer cells, has been believed a driving force for genetic instability in the development of cancer and received extensively exploration in recent years. In our previous work, we have demonstrated that TEIF（transcriptional elements-interacting factor）distributes at the centrosome and regulates its status in physiological condition, DNA damage response or carcinogenesis. Here, we further expand our knowledge of TEIF to the downstream effector of EGF/PI3K/Akt signaling. The addition of EGF or transfection of active Akt stimulated TEIF expression, resulting in an increase of centrosome splitting and amplification, while the inhibitors of either PI3K or Akt attenuated the changes in TEIF and its associated centrosome status. A consensus motif for Akt phosphorylation (RHRVLT) was revealed in TEIF domain of localizing at the centrosome and identified as the site for phosphorylation of TEIF both in vitro and in vivo experiments, indicating TEIF as a direct substrate to Akt1. Furthermore, in a collection of aggressive breast cancers a positive correlation between the expression of TEIF and centrosome amplification was clarified and also closely concerned to the over-expression of CerbB2 (a member of EGFR family) and the level of phosphorylated Akt (pAkt) in cancer tissues. These findings not only could link EGF/PI3K/Akt oncogenic signaling with centrosome amplification, but also could provide more choices in the development of specific inhibitors for anti-cancer therapeutic agents targeting to EGF/PI3K/Akt signaling.
	TO cite this article:ZHAO Jing,CHI Yingkai,LIU Haijing, et al. TEIF associated centrosomal activity is regulated by EGF/PI3K/Akt signaling[OL].[11 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4461460


	5. A small interfering RNA targeting NF-kappaB p65 alone or combined with 5-FU inhibits the growth of esophageal squmous cell carcinoma in nude mice
	TIAN Fang,FAN Tianli,JIANG Yanan,ZHANG Xiaoyan,WANG Xinhua
	Basic Medicine 07 November 2011
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	Abstract:NF-κB signaling pathway plays an important role in carcinogenesis. Although constitutive NF-κB activation has been reported in many human tumors, the effect of NF-κB signaling pathway in esophageal squamous cell carcinoma (ESCC) is still poorly understood. To explore the role of NF-κB signaling pathway in ESCC, RNA interference (RNAi) was used to knockdown NF-κB p65 protein level in the ESCC cells and in nude mice. 5-FU was used to investigated whether knockdown NF-κB p65 can potentiate 5-FU's antitumor effect. Animal results indicated that the tumor growth was inhibited in p65 siRNA and p65 siRNA + 5-FU groups compared with control group. Immunohistochemistry, RT-PCR and TUNEL assay showed that p65 siRNA downregulated the expression of p65 and enhanced the sensitivity of EC9706 cells to 5-FU treatment in vivo. Overall, our work indicated that downregulation of p65 can increase the tumor apoptosis and potentiates the effects of 5-FU by suppressing NF-κB signaling pathway. Thus, p65 is an interesting target for ESCC treatment.
	TO cite this article:TIAN Fang,FAN Tianli,JIANG Yanan, et al. A small interfering RNA targeting NF-kappaB p65 alone or combined with 5-FU inhibits the growth of esophageal squmous cell carcinoma in nude mice[J].


	6. The research about REIC expression and its correlation with clinicopathological parameters of gastric carcinomas
	Xu Xiaoyan,Xia Pu,Zheng Huachuan
	Basic Medicine 27 October 2011
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	Abstract:REIC is down-regulated in immortalized cell lines compared with the parental normal counterparts. It may inhibit colony formation, tumor growth, and induce the apoptosis. Here, REIC expression was examined in gastric carcinomas by RT-PCR, Western blot and immunohistochemistry, and compared with clinicopathological parameters of carcinoma. Immunohistochemically, REIC expression was negatively associated with tumor size, lymph node metastasis, dedifferentiation or poor prognosis of carcinoma. These results suggest that REIC expression may be a promising objective and effective marker to predict pathobiological behaviors and prognosis of gastric carcinoma.
	TO cite this article:Xu Xiaoyan,Xia Pu,Zheng Huachuan. The research about REIC expression and its correlation with clinicopathological parameters of gastric carcinomas[OL].[27 October 2011] http://en.paper.edu.cn/en_releasepaper/content/4447599


	7. The expression and significance of androgen receptor in HBV-associated chronic liver diseases
	Zhu Rong,Gu Dong-Hua
	Basic Medicine 20 January 2011
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	Abstract:Purpose:To explore the AR and HBx expression in both mRNA levels and protein levels, and to find the relationship among them and clinical characteristics. Compared with the negative controls, we tried to find the role of AR in HBV-associated hepatocarcinogenesis. Methods: Eighty-three cases of surgically resected HBV-associated HCC and 14 cases of the HBV-negative HCC were selected. Meanwhile, 13 peritumoral liver tissues from hemangioma served as benign control. One hundred and eighty-nine liver biopsy samples of chronic hepatitis B and 75 cases whose diagnosis as "No pathological diagnostic abnormal" were also selected. The expressions at mRNA levels were detected by fluorescence quantitative real-time RT-PCR. Western blot and En Vision immunohistochemical stain investigated the protein expressions. Results: In 83 HBV-associated HCC cases, in both peritumoral tissues (P=0.000) and tumors (P=0.000), AR mRNA levels correlated positively with HBx; The expression of AR (P=0.011) and HBx (P=0.000) was significantly higher in peritumoral tissues than in tumors; HBV-associated HCC cases had significantly higher AR mRNA than HBV-negative HCC in both peritumoral tissues (P=0.027) and tumors (P=0.021). The results from western blot analysis and Immunohistochemical stain were consistent with those of mRNA levels.In chronic hepatitis B patients, the expression of AR correlated with the grade of Scheuer scores (P=0.034). Conclusions: To clarified the expression of AR in HBV-associated HCC and chronic hepatitis B cases. AR plays a role in HBV-associated hepatocarcinogenesis. HBx-induce AR expression may be a mechanism of hepatocarcinogenesis. AR had stronger expression in peritumoral tissues than in tumors implied that the expression of AR increases during preneoplastic stages and that progression towards cancer development can suppress maintain AR expression levels. It is therefore proposed that androgen therapy may be ineffective after establishment of tumor. In chronic hepatitis B, AR pathway may be related with inflammation.
	TO cite this article:Zhu Rong,Gu Dong-Hua. The expression and significance of androgen receptor in HBV-associated chronic liver diseases[OL].[20 January 2011] http://en.paper.edu.cn/en_releasepaper/content/4408010


	8. More mesenchymal stem cells are recovered from bone marrow aspirates by culturing bone marrow particles and mononuclear cells respectively
	Xing Wen,Liu Pengxia,Liu Meng,Yang Shaoguang,Zhao Qinjun,Li Jianping,Lu Shihong,Ren Hongying,Han Zhongchao
	Basic Medicine 04 January 2011
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	Abstract:Bone marrow (BM) is the major source of mesenchymal stem cells (MSCs). In most experiments, MSCs were classically cultured from mononuclear cells (MNCs) isolated by density gradient centrifugation method. However, several groups have demonstrated that this method was less efficient for MSCs' recovery. Here, we investigated whether BM particles were the cause and how to isolate them. A total of 20 patients were enrolled. MNCs were cultured by standard adherence and BM particles were cultivated by primary explant culture. For BM from patients 1-10, we first isolated MNCs, then filtered out BM particles. We then compared the morphology and the fibroblastic colony number between cultures of MNCs and BM particles. For BM from patients 11-20, we processed them in opposite order. We then compared the immunophenotype and function between adherent cells expanded from MNCs and BM particles. In addition, for patients 11-20，we cultured the left BM aspirates after BM particles and MNCs were isolated respectively. Adherent cells from BM particles were MSCs. After BM particles were filtered out and cultured separately, MSCs could be recovered completely from MNCs isolated by density gradient centrifugation and no MSCs were left in the residual BM aspirates. BM particles, which have been mostly discarded by the method of density gradient centrifugation, are another important source of MSCs and they can be cultivated reliably by primary explant culture. More MSCs are recovered from a single BM sample by culturing BM particles and MNCs respectively.
	TO cite this article:Xing Wen,Liu Pengxia,Liu Meng, et al. More mesenchymal stem cells are recovered from bone marrow aspirates by culturing bone marrow particles and mononuclear cells respectively[J].


	9. The correlation of fascin over-expression with motility and invasion of tumor cells
	Li Weiping,Ma Gui
	Basic Medicine 12 November 2010
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	Abstract:In the progression of the cancer invasion, carcinoma cells migrate away from primary tumors, traverse to basement membrane and extracellular matrix (ECM), overcome the cell-cell and cell-ECM adhesions, invade surrounding tissue, and come into the metastases through lymphatic and/or blood system .Of all these processes, the acquisition and increase of cell motile and invasive properties play a crucial role in the neoplasm progression. Fascin, an Actin-bundling protein, is considered to induce specific morphological features of membrane protrusion, as well as the changes of cell adhesion and cell interactions, and ultimately enhance the cell motility for subsequent invasion and metastasis, which is significantly negatively correlated with prognosis and survival rate. It is profound to study the involvement of fascin in the mechanism of invasion and metastasis so as to provide effective early diagnosis for potentially aggressive tumors or be used to develop therapeutic strategies that can arrest invasion and even metastases.
	TO cite this article:Li Weiping,Ma Gui. The correlation of fascin over-expression with motility and invasion of tumor cells[OL].[12 November 2010] http://en.paper.edu.cn/en_releasepaper/content/4391408


	10. The motility and invasion of tumor cell and its association with Fascin
	Ma Gui,Li WeiPing
	Basic Medicine 11 June 2010
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	Abstract:In the progression of the cancer, carcinoma cells migrate away from primary tumors, traverse to basement membrane and ECM, overcome the cell-cell and cell-ECM adhesions, invade surrounding tissue, and come into the metastases through lymphatic and/or blood system .Of all these processes, the acquisition and increase of cell motile and invasive properties play a crucial role in the neoplastic progression. Fascin, as an Actin-bundling protein, is prevalently considered to induce specific morphological features of membrane protrusion, as well as the changes of cell adhesion and cell interactions, and ultimately enhance the cell motility for subsequent invasion and metastases, which is significantly associated with bad prognosis. Therefore, fascin over-expression is proposed to be a novel biomarker to provide effective early diagnosis for potentially aggressive tumors or be used to develop therapeutic strategies that can arrest invasion and even metastases.
	TO cite this article:Ma Gui,Li WeiPing. The motility and invasion of tumor cell and its association with Fascin[OL].[11 June 2010] http://en.paper.edu.cn/en_releasepaper/content/4376011

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