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| 1 | CCK-8法与MTT法检测人前列腺癌PC3细胞活性的比较研究显示文摘目的探讨CCK-8法和MTT法的最佳实验条件。方法以人前列腺癌PC3细胞作为研究对象,采用CCK-8和MTT法检测抗肿瘤药物阿霉素(ADM)对PC3细胞增殖的影响。结果 CCK-8法的最佳检测波长为450 nm,最佳检测时间为加入CCK-8试剂后4 h,适宜细胞数量范围为8×102~1×105个。结论 CCK-8法较MTT法检测的灵敏度高,准确性好,是一种优于MTT法的检测细胞增殖活性的方法。 | 万文婷 李宁 刘静 金林红 | 2010 | 时珍国医国药2010，21，12： | 31 |
| 2 | FoxO3a and disease progression显示文摘The Forkhead box O(FoxO) family has recently been highlighted as an important transcriptional regulator of crucial proteins associated with the many diverse functions of cells. So far, FoxO1, FoxO3 a, FoxO4 and FoxO6 proteins have been identified in humans. Although each FoxO family member has its own role, unlike the other FoxO families, FoxO3 a has been extensively studied because of its rather unique and pivotal regulation of cell proliferation, apoptosis, metabolism, stress management and longevity. FoxO3 a alteration is closely linked to the progression of several types of cancers, fibrosis and other types of diseases. In this review, we will examine the function of FoxO3 a in disease progression and also explore FoxO3a's regulatory mechanisms. We will also discuss FoxO3 a as a potential target for the treatment of several types of disease. | Richard Seonghun Nho Polla Hergert | 2014 | World Journal of Biological Chemistry2014，5，3： | 28 |
| 3 | Inhibitory effect of norcantharidin on the growth of human gallbladder carcinoma GBC-SD cells in vitro显示文摘 | Fan, Yue-Zu Fu, Jin-Ye Zhao, Ze-Ming Chen, Chun-Qiu | 2007 | Hepatobiliary & Pancreatic Diseases International2007，6，1： | 25 |
| 4 | Effects of salvianolic acid-A on NIH/3T3 fibroblast proliferation,collagen synthesis and gene expression显示文摘AIM To investigate the mechanisms ofsalvianolic acid A(SA-A)against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely,and incubated with 10-4mol/L-10-7mol/L SA-A for 22 h.The cell viability wasassayed by[3H]proline incorporation,cellproliferation by[3H]TdR incorporation,cellcollagen synthetic rate was measured with[3H]proline impulse and collagenase digestionmethod.The total RNA was prepared from thecontrol cells and the drug treated cellsrespectively,and α(1)I pro-collagen mRNAexpression was semi-quantitatively analyzedwith RT-PCR.RESULTS 10-4mol/L SA-A decreased cellviability and exerted some cytotoxiciy,while10-5mol/L-10-7mol/L SA-A did not affect cellviability,but inhibited cell proliferationsignificantly,and 10-6mol/L SA-A had the besteffect on cell viability among theseconcentrations of drugs.10-5mol/L-10-6mol/LSA-A inhibited intracellular collagen syntheticrate,but no significant influence on extracellularcollagen secretion.Both 10-5mol/L and10-6mol/L SA-A could decrease α(1)I pro-collagen mRNA expression remarkably.CONCLUSION SA-A had potent action againstliver fibrosis.It inhibited NIH/3T3 fibroblastproliferation,intracellular collagen syntheticrate and type I pro-collagen gene expression,which may be one of the main mechanisms of thedrug. | Liu CH Hu YY Wang XL Liu P Xu LM | 2000 | World Journal of Gastroenterology2000，6，3： | 25 |
| 5 | Effects of ginsenoside Rh2 on growth and migration of pancreatic cancer cells显示文摘AIM:To investigate the effects of ginsenoside Rh2 on the human pancreatic cancer cell line Bxpc-3.METHODS:The human pancreatic cancer cell line Bxpc-3 was cultured in vitro and treated with or without ginsenoside Rh2.Growth rates for Bxpc-3 cells were assessed by methyl thiazolyl tetrazolium(MTT) and colony formation assays.Cell cycle changes were analyzed by flow cytometry.Apoptosis was measured by flow cytometry and Hoechst 33258 fluorescence staining.A scratch assay and a Matrigel invasion assay were used to detect cell migration and invasion.Expression of Bax,Bcl-2,survivin,cyclin D1,matrix metalloproteinase(MMP)-2,MMP-9,cleaved caspase-3,caspase-8,and caspase-9 mRNA were determined by reverse transcriptase-polymerase chain reaction(RT-PCR).Bax,Bcl-2,survivin,cyclin D1,cleaved caspase-3,caspase-8 and caspase-9 protein levels were examined by western blotting.Expression of MMP-2 and MMP-9 proteins in culture supernatants were determined by enzymelinked immunosorbent assay(ELISA).RESULTS:Rh2 significantly inhibited Bxpc-3 cell proliferation in a dose-and time-dependent manner,as evaluated by the MTT(P < 0.05) and colony formation assays(P < 0.05).Compared to the control group,Rh2 significantly increased the percentage of Bxpc-3 cells in the G 0 /G 1 phase from 43.32% ± 2.17% to 71.32% ± 1.16%,which was accompanied by a decrease in S phase(from 50.86% ± 1.29% to 28.48% ± 1.18%) and G 2 /M phase(from 5.81% ± 1.19% to 0.20% ± 0.05%) in a dose-dependent manner(P < 0.05),suggesting that Rh2 arrested cell cycle progression at the G 0 /G 1 phase,as measured by flow cytometry.Compared to the control group,cells treated with Rh2 showed significantly higher apoptosis ratios in a dosedependent manner(percentage of early apoptotic cells:from 5.29% ± 2.28% to 38.90% ± 3.42%(F = 56.20,P < 0.05);percentage of late apoptotic cells:from 4.58% ± 1.42% to 36.32% ± 2.73%(F = 86.70,P < 0.05).Rh2 inhibited Bxpc-3 cell migration and invasion,as detected by scratch wound healing assay and Matrigel invasion assay [percentages of scratch wound healing for 12 h,24 h and 48 h(control vs experimental group):37.3% ± 4.8%vs 18.30% ± 1.65%,58.7% ± 3.5% vs 38.00% ± 4.09% and 93.83% ± 4.65% vs 65.50% ± 4.09%,respectively;t = 6.489,t = 6.656 and t = 7.926,respectively,P < 0.05;the number of cells invading at various concentrations(0 μmol/L,35 μmol/L,45 μmol/L and 55 μmol/L):81.10 ± 9.55,46.40 ± 6.95,24.70 ± 6.88 and 8.70 ± 3.34,respectively(F = 502.713,P < 0.05)].RT-PCR,western blotting or ELISA showed that mRNA and protein expression of Bax,cleaved caspase-3 and caspase-9 were upregulated(P < 0.05),while mRNA and protein expression of Bcl-2,survivin,cyclin D1,MMP-2 and MMP-9 were downregulated(P < 0.05).CONCLUSION:Ginsenoside Rh2 inhibits proliferation,migration and invasion and induces apoptosis of the human pancreatic cancer cell line Bxpc-3. | Xi-Ping Tang Guo-Du Tang Chun-Yun Fang Zhi-Hai Liang Lu-Yi Zhang | 2013 | World Journal of Gastroenterology2013，19，10： | 19 |
| 6 | Effect of lipid on proliferation and activation of rat hepatic stellate cells(Ⅰ)显示文摘INTRODUCTIONDespitetheearlycontroversyovertheprimarycelularsourceofextracelularmatrixproteinsinliverfibrosis,compelinginvitro... | LU Lun Gen, ZENG Min De, LI Ji Qiang, HUA Jing, FAN Jian Gao, FAN Zhu Ping and QIU De Kai | 1998 | World Journal of Gastroenterology1998，4，6： | 18 |
| 7 | Hepatitis B virus X protein promotes proliferation and upregulates TGF-β1 and CTGF in human hepatic stellate cell line,LX-2显示文摘BACKGROUND:Chronic hepatitis B virus(HBV)infection is a major cause of liver fibrosis,but the mechanisms underlying HBV-related fibrogenesis are still unknown. Although the roles of HBV X protein(HBx)remain poorly understood,it is thought to play an important role in the regulation of cellular growth and hepatocarcinogenesis. The aim of this study was to determine the role of HBx in liver fibrogenesis by studying the effect of HBx on the proliferation and expression of fibrosis-related molecules in the human hepatic stellate cell line,LX-2. METHODS:We established an in vitro co-culture system with LX-2 cells and a stable QSG7701-HBx cell line which had been transfected with the HBx gene. 3 H-TdR incorporation and flow cytometry were used to determine the effects of HBx on the proliferation of LX-2 cells. α-smooth muscle actin(α-SMA),transforming growth factor-β1(TGF-β1),transforming growth factor-βreceptor Ⅱ(TGF-βRⅡ),and connective tissue growth factor (CTGF)in LX-2 cells were analyzed by Western blotting.In addition,the expression levels of collagen typeⅠ(ColⅠ) from the co-cultured media were measured by ELISA. RESULTS: 3 H-TdR incorporation increased significantly in LX-2 cells co-cultured with QSG7701-HBx cells compared to those cultured with QSG7701-pcDNA3 and QSG7701 (non-tumorigenic human liver cell line).Cell cycle results revealed that HBx accelerated the progression of G1 to S in LX-2 cells.The expressions ofα-SMA,TGF-β1,TGF-βRⅡ,CTGF and ColⅠwere significantly increased in the co- cultures of LX-2 cells with stable QSG7701-HBx cells. CONCLUSION:These results suggest that HBx may facilitate liver fibrosis by promoting hepatic stellate cell proliferation and upregulating the expression of fibrosis- related molecules. | Guang-Hui Guo,De-Ming Tan,Ping-An Zhu and Fei Liu Department of Infectious Diseases,Xiangya Hospital,Central South University,Changsha 410008,China | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，1： | 17 |
| 8 | Effect and molecular mechanism of mir-146a on proliferation of lung cancer cells by targeting and regulating MIF gene显示文摘Objective: To discuss the effect and molecular mechanism of mi R-146 a on the proliferation of lung cancer cells by targeting and regulating the macrophage migration inhibitory factor(MIF) gene. Methods: RT-PCR was employed to detect expression of mi R-146a; immunohistochemistry was used to detect the expression of MIF. The luciferase reporter gene technique was adopted to verify that MIF was the specific reverse target gene of mi R-146 a and the liposome LipofectamineTM2000 was employed to transfer the modeled mi R-146 a mimics, and mi R-146 a negative control(NC) in NSCLC cells to detect the expression of MIF m RNA and protein. MTT assay was used to detect cell viability, cloning technique to detect cell proliferation ability, Annexin V-PI to detect cell apoptosis, UV spectrophotometry to detect viability of cysteinyl aspartate specific proteinase 3(Caspase 3), and western blot to detect expression of nuclear factor-κB(NF-κB) in cells. Results: The expression of mi R-146 a in NSCLC lung tissues was lower than that in the normal lung tissues besides the lung cancer; while the expression of mi R-146 a in NSCLC cells was lower than that in normal human embryonic lung tissues. It was chosen as the subsequent cell line for its appropriate expression in A549. The expression of MIF protein in NSCLC lung tissues was higher than that in the normal lung tissues besides the lung cancer. The luciferase reporter gene proved that MIF was the reverse target gene of mi R-146 a. The mi R-146 a mimics were transfected into A549 cells through the liposome. Compared with NC group, the expression of MIF protein and m RNA was significantly decreased(P<0.01), with the decrease in the cell viability(P<0.01), the decrease in the number of clones(P<0.01), cell apoptosis(P<0.01), the increase in the activity of Caspase 3(P<0.01), and decrease in the phosphorylation of NF-κB p65(P<0.01). Conclusions: mi R-146 a has low expression in NSCLC tissues and cell lines, while MIF has the over expression in NSCLC tissues. The increased expression of mi R-146 a can inhibit the expression of MIF via the gene targeting and thus inhibit the proliferation of A549 cells and induce the apoptosis of cancer cells, which may be realized through NF-κB signaling pathway. | Wu-Ming Wang Ji-Chun Liu | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，8： | 17 |
| 9 | Inhibitory effects of Curcuma aromatica oil on proliferation of hepatoma in mice显示文摘AIM To reveal the inhibitory effects ofCurcuma aromatica oil(CAO)on cellproliferation of hepatoma in mice.METHODS Two tumor inhibitory experimentsof CAO on hepatoma in mice were conducted.The inhibitory effects of CAO on proliferation ofhepatoma in mice were evaluated by DNA imagecytometry and immunohistochemical staining ofproliferating cell nuclear antigen(PCNA).RESULTS The tumor inhibitory rates of CAOwere 52% and 51% in two experiments,respectively.Compared with those of the saline-treated control groups,both differences werestatistically significant(P<0.01).In the groupof mice treated with CAO,the cellular nuclearDNA OD value(249±70),areas(623 μm^2±228 μm^2)and DNA(2.38±0.67)index of hepaticcarcinomas were significantly lower than thoseof the control group(430±160,1073 μm^2±101 μm^2 and 4.48±0.71).CAO also couldincrease diploidy cell rates(29.00%±9.34% vs2.97%±5.69%,P<0.01)and decreasepentaploidy cell exceeding rate(30.04%±15.10% vs 70.89%±14.94%,P<0.01).In thegroup of mice treated with CAO,the labelingindexes of proliferating cell nuclear antigen (PCNA-LI)were 30%±4%,which weresignificantly lower than 40%±6% of the controlgroup(P<0.01).CONCLUSION The inhibition of CAO on thegrowth of hepatoma in mice might be associatedwith its depression on cellular proliferativeactivity. | Wan Yin Wu Qin Xu Ling Chun Shi Wei Bin Zhang | 2000 | World Journal of Gastroenterology2000，6，2： | 16 |
| 10 | Effect of Helicobacter pylori infection on gastric epithelial cell proliferation显示文摘INTRODUCTION Helicobacter pylori(H.pylori)infection is one ofthe main pathogens of chronic gastritis and duodenalulcer(DU),and it may be considered as a riskfactor in the incidence of gastric cancer.H.pylori infection may lead to the anomaly of gastricepithelial cell proliferation which is closely relatedto the development of gastric cancer.Vacuolatingcytotoxin(VacA)is an important virulence andvacA subtype determines the toxic activity.According to its signal sequence,it can be groupedinto type sla,slb,slc and s2.Strains harboringvacAsla are more closely related with digestivediseases and may be the strains with high toxicity.The effect of H.pylori infection on | Gao H Wang JY Shen XZ Liu JJ | 2000 | World Journal of Gastroenterology2000，6，3： | 14 |
| 11 | S100B protein in tissue development,repair and regeneration显示文摘The Ca 2+-binding protein of the EF-hand type,S100B,exerts both intracellular and extracellular regulatory activities.As an intracellular regulator,S100B is involved in the regulation of energy metabolism,transcription,protein phosphorylation,cell proliferation,survival,differentiation and motility,and Ca 2+ homeostasis,by interacting with a wide array of proteins(i.e.,enzymes,enzyme substrates,cytoskeletal subunits,scaffold/adaptor proteins,transcription factors,ubiquitin E3 ligases,ion channels) in a restricted number of cell types.As an extracellular signal,S100B engages the pattern recognition receptor,receptor for advanced glycation end-products(RAGE),on immune cells as well as on neuronal,astrocytic and microglial cells,vascular smooth muscle cells,skeletal myoblasts and cardiomyocytes.However,RAGE may not be the sole receptor activated by S100B,the protein being able to enhance bFGF-FGFR1 signaling by interacting with FGFR1-bound bFGF in particular cell types.Moreover,extracellular effects of S100B vary depending on its local concentration.Increasing evidence suggests that at the concentration found in extracellular fluids in normal physiological conditions and locally upon acute tissue injury,which is up to a few nM levels,S100B exerts trophic effects in the central and peripheral nervous system and in skeletal muscle tissue thus participating in tissue homeostasis.The present commentary summarizes results implicating intracellular and extracellular S100B in tissue development,repair and regeneration. | Guglielmo Sorci Francesca Riuzzi Cataldo Arcuri Claudia Tubaro Roberta Bianchi Ileana Giambanco Rosario Donato | 2013 | World Journal of Biological Chemistry2013，4，1： | 14 |
| 12 | Role of IL-10 in the progression of kidney disease显示文摘Interleukin-10(IL-10), a cytokine with anti-inflammatory and immunomodulatory functions, regulates the biology of B and T cells. The present review describes the role of IL-10 in normal renal physiology, during acute kidney injury and in the development of chronic renal failure. We further discuss IL-10-induced cellular and molecular pathways and their link to the progression of kidney injury. | Inna Sinuani Ilia Beberashvili Zhan Averbukh Judith Sandbank | 2013 | World Journal of Transplantation2013，3，4： | 11 |
| 13 | Potential roles of EZH2, Bmi-1 and mi R-203 in cell proliferation and invasion in hepatocellular carcinoma cell line Hep3B显示文摘AIM: To investigate the potential roles of enhancer of zeste homolog2(EZH2), Bmi-1 and mi R-203 in cell proliferation and invasion in hepatocellular carcinoma(HCC) cell line Hep3 B.METHODS: A total of 73 patients who underwent surgical resection at Fuzong Clinical Medical College of Fujian Medical University were enrolled in this study. Hep3 B cells were cultivated in RPMI 1640 medium supplemented with 10% fetal bovine serum at 37?℃. Vectors that containing c DNA of the EZH2 gene or mi R-203 targeted sh RNA plasmid were constructed, and then transfected into Hep3 B cells. The m RNA expression of mi R-203, EZH2, and Bmi-1 was analyzed using quantitative real-time polymerase chain reaction analysis, and the protein levels of EZH2 and Bmi-1 were detected by Western blot analysis. Effect of EZH2 or mi R-203 on cell proliferation was observed by methyl thiazolyl tetrazolium assay, and cell apoptosis was assessed using flow cytometry. Besides, effect of EZH2 or mi R-203 on tumor cell invasion was detected using Transwell assay.RESULTS: The m RNA levels of EZH2 and Bmi-1 in HCC tissues and in Hep3 B cells were significantly higher compared with those in normal samples(P < 0.01), while mi R-203 level was significantly lower in HCC tissues(P < 0.01). Hep3 B cells transfected with EZH2-sh RNA or mi R-203-sh RNA showed lower expression levels of EZH2 and Bmi-1(P < 0.05). Compared with controls, Hep3 B cells transfected with EZH2-sh RNA had relative slow cell proliferation, indicating that low expression of EZH2 and Bmi-1 and overexpression of mi R-203 could inhibit Hep3 B cell proliferation(P < 0.05). The average apoptosis rate of Hep3 B cells transfected with EZH2-sh RNA vector was about 18.631%, while that of Hep3 B cells transfected with sh RNA vector was about 5.33%, suggesting that EZH2 was down-regulated by transfecting with EZH2-sh RNA, and the down-regulated EZH2 contributed to the cell apoptosis. Low expression of EZH2 and Bmi-1 and overexpression of mi R-203 could reduce Hep3 B cell invasion(P < 0.05).CONCLUSION: Our study suggests that EZH2 and Bmi-1 are up-regulated while mi R-203 is downregulated in Hep3 B cells. Mi R-203 may contribute to the metastasis and enhance apoptosis of HCC cells by regulating EZH2 and Bmi-1. Our study may provide a theoretical basis for metastasis of HCC and targeted therapy of HCC. | Fang Yang Li-Zhi Lv Qiu-Cheng Cai Yi Jiang | 2015 | World Journal of Gastroenterology2015，21，47： | 11 |
| 14 | Effect of WFDC 2 silencing on the proliferation,motility and invasion of human serous ovarian cancer cells in vitro显示文摘Objective:To investigate effect and possible mechanisms of silencing human WFDC2(HE4) gene on biological behavior changes as cell proliferation,apoplosis,movement and invasion of human serous ovarian cancer cell line SKOV3.Methods:Lentiviral WFDC2 gene sequence of small interfering siRNA was stablely transfected into SKOV3 identified by Q-PCR and western-blot. Obtained SKOV3 stable strains with silenced HE4 were measured by proliferation,apoplosis, migration,and invasion.Results:Gene sequencing showed that the oligonucleotides were successfully inserted into the expected site.After silencing HE4 in the SKOV3,proliferation was significandy inhibited(P<0.05).G0/G1 phase was arrested by the cell cycle(P<0.01) and capacity of the migration and invasion decreased significandy(P<0.01).Slight early apoptosis ratio and no change of late apoplosis were found without change of Caspase-3 or Bcl-2 protein.Proteins involed in ERK pathway as phosphorylated protein as p-EGFR,p- ERK decreased and protease protein involved in tissue remoding as matrix metalloproteinases MMP-9,MMP-2 and cathepsin B decreased compared with control group.Conclusions:HE4 gene plays an important role in regulating proliferation,apoptosis,migration,invasion of serous ovarian cancer cells by ERK pathway and protease system.Its role in apoptosis needs to be further explored,and it may be a potential target for serous ovarian cancer. | Ya-Fei Zhu Guo-Lan Gao Sheng-Bo Tang Zhen-Dong Zhang Qing-Shui Huang | 2013 | Asian Pacific Journal of Tropical Medicine2013，6，4： | 11 |
| 15 | Anticancer effects of sweet potato protein on human colorectal cancer cells显示文摘AIM: To investigate the effects of proteins purified from sweet potato storage roots on human colorectal cancer cell lines. METHODS: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Hoechst 33258 nuclear staining and Boyden transwell chamber methods were used to determine whether purified sweet potato protein (SPP) from fresh sweet potato roots affected proliferation, migration and invasion, respectively, of human colorectal cancer SW480 cells in vitro . The inhibitory effects of SPP on growth of human colorectal cancer HCT-8 cells intraperitoneally xenografted in nude mice and spontaneous lung metastasis of murine Lewis lung carcinoma 3LL cells subcutaneously transplanted in C57 BL/6 mice were also investigated in vivo . RESULTS: SPP inhibited the proliferation of SW480 cells in a dose-dependent manner, with an IC 50 value of 38.732 μmol/L (r2 = 0.980, P = 0.003) in the MTT assay. Hoechst 33258 nuclear staining further revealed inhibition of cell viability and induction of apoptosis by SPP. The transwell assay disclosed significant reduction in migrated cells/field by 8 μmol/L SPP (8.4 ± 2.6 vs 23.3 ± 5.4, P = 0.031) and invaded cells/field through the ECMatrix by 0.8 μmol/L SPP, compared with the control (25.2 ± 5.2 vs 34.8 ± 6.1, P = 0.038). Both intraperitoneal (ip) and intragastric (ig) administration of SPP led to significant suppression of growth of intraperitoneally inoculated HCT-8 cells in nude mice to 58.0% ± 5.9% (P = 0.037) and 43.5% ± 7.1% (P = 0.004) of the controls, respectively, after 9 d treatment. Bloody ascites additionally disappeared after ip injection of trypsin inhibitor. Notably, ig and ip administration of SPP induced a significant decrease in spontaneous pulmonary metastatic nodule formation in C57 BL/6 mice (21.0 ± 12.3 and 27.3 ± 12.7 nodules/lung vs 42.5 ± 4.5 nodules/lung in controls, respectively, P < 0.05) after 25 d treatment. Moreover, the average weight of primary tumor nodules in the hind leg of mice decreased from 8.2 ± 1.3 g/mice in the control to 6.1 ± 1.4 g/mice in the ip group (P = 0.035). CONCLUSION: SPP exerts significant antiproliferative and antimetastatic effects on human colorectal cancer cell lines, both in vitro and in vivo . | Peng-Gao Li Tai-Hua Mu Le Deng | 2013 | World Journal of Gastroenterology2013，19，21： | 9 |
| 16 | Role of free fatty acids in proliferation of rat hepatic stellate cells(Ⅱ)显示文摘INTRODUCTIONAlthoughtheroleofhepatocytesinfatyacidsmetabolismandtransporthavebeendiscusedintensively,fewofthatofHSCwasreporte... | LU Lun Gen, ZENG Min De, LI Ji Qiang, HUA Jing, FAN Jian Gao and QIU De Kai | 1998 | World Journal of Gastroenterology1998，4，6： | 8 |
| 17 | Diabetes inhibits corneal epithelial cell migration and tight junction formation in mice and human via increasing ROS and impairing Akt signaling显示文摘Corneal wounds usually heal quickly;but diabetic patients have more fragile corneas and experience delayed and painful healing. In the present study, we compared the healing capacity of corneal epithelial cells (CECs) between normal and diabetic conditions and the potential mechanisms. Primary murine CEC derived from wild-type and diabetic (db/db) mice, as well as primary human CEC were prepared. Human CEC were exposed to high glucose (30 mM) to mimic diabetic conditions. Cell migration and proliferation were assessed using Scratch test and MTT assays, respectively. Reactive oxygen species (ROS) production in the cells was measured using dichlorofluorescein reagent. Western blot was used to evaluate the expression levels of Akt. Transepithelial electrical resistance (TEER) and zonula occludens-1 (ZO-1) expression were used to determine tight junction integrity. We found that the diabetic CEC displayed significantly slower cell proliferation and migration compared with the normal CEC from both mice and humans. Furthermore, ROS production was markedly increased in CEC grown under diabetic conditions. Treatment with an antioxidant N-acetyl cysteine (NAC, 100 μM) significantly decreased ROS production and increased wound healing in diabetic CEC. Barrier function was significantly reduced in both diabetic mouse and human CEC, while NAC treatment mitigated these effects. We further showed that Akt signaling was impaired in diabetic CEC, which was partially improved by NAC treatment. These results show that diabetic conditions lead to delayed wound-healing capacity of CEC and impaired tight junction formation in both mice and human. Increased ROS production and inhibited Akt signaling may contribute to this outcome, implicating these as potential targets for treating corneal wounds in diabetic patients. | Qi-wei Jiang Denis Kaili Jonaye Freeman Chong-yang Lei Bing-chuan Geng Tao Tan Jian-feng He Zhi Shi Jian-jie Ma Yan-hong Luo Heather Chandler Hua Zhu | 2019 | Acta Pharmacologica Sinica2019，40，9： | 8 |
| 18 | MicroRNA-184 promotes proliferation ability of glioma cells by regulating FOXO3显示文摘Objective:To investigate the effect of microRNA(miR-184)on regulating the genesis.development and prolifration of glioma cells.Methods:Lipidosome was used to transfect miR-184 mimic and inhibitor to glioma cell ling,and the cell proliferation ability changes were determined by MTT and plate cloning experiment after the transfection.WB test was used to measure the levels of cyclinD1,p27 and FOXO3.Meanwhile.QPCR was used to detect miR-184expression in glioma cell line.glioma tissues and adjacent tissues.Luciferase experiment was used to test 3'UTR gene targeting regulation of miR-184 and FOXO3.Results:QPCR results showed a significaat lower miR-184 expression level in glioma cell line and glioma tissues than that in juxtacancerous tissue.MTT and plate cloning experiments have shown that after overexpressing of miR-184,the cell proliferation capacity of glioma U87 and T98G was signifieantly increased,which was significantly inhibited after the inhibition of miN-184.WB results showed a lower expression level of p27 in U87 and T98G cells,and a higher expression level of cyclind1after over-expressing of miR-184 wss observed.However.a lower expression level of eyelinD1and a higher expression level of p27 after the inhibition of miR-184.The luciferase activity was inhibited after the over-expressing of miR-184.Conclusions:MiR-184 can affect the proliferation abilities of glioma cells and regulate the cell cycle related protein.It plays an important role in the occurrence and development of gliomas. | Qing-Ke Cui Wei-Dong Liu Jian-Xin Zhu Yun-Hua Wang Zhi-Gang Wang | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，10： | 7 |
| 19 | NIMA related kinase 2 promotes gastric cancer cell proliferation via ERK/MAPK signaling显示文摘BACKGROUND NIMA related kinase 2(NEK2) is closely related to mitosis, and it is currently considered to be over-expressed frequently in many poorly prognostic cancers.However, the effect of the up-regulated NEK2 on cellular signaling in tumors,such as gastric cancer(GC), is con-fusing.AIM To determine the role of the up-regulation of NEK2 in GC.METHODS To investigate the pathological significance of NEK2 in GC, the expression pattern of NEK2 in GC was investigated based on the 'Oncomain' database and compared between 30 pairs of cancer samples and adjacent tissues. The coexpression of NEK2 and ERK in GC was analyzed using The Cancer Genome Atlas(TCGA) database and confirmed in clinical samples by quantitative realtime PCR(qRT-PCR), and the survival curve was also plotted. Western blot or qRT-PCR was used to analyze the effect of NEK2 on the phosphorylation levels of ERK and c-JUN in two GC cell lines(BGC823 and SGC7901) with NEK2 overexpression, and the expression of the downstream effector cyclin D1.Furthermore, CCK8, EdU incorporation assay, and flow cytometry were used to detect the proliferative ability of BGC823 and SGC7901 cells with stably silenced ERK.RESULTS NEK2 was significantly up-regulated in human GC tissues. ERK was significantly associated with NEK2 expression in human clinical specimens, and combined overexpression of NEK2 and ERK potentially forecasted a poor prognosis andsurvival in GC patients. NEK2 knockdown in GC cells inhibited ERK and c-JUN phosphory-lation and reduced the transcription of cyclin D1. More interestingly,NEK2 can rescue the inhibition of cellular viability, proliferation, and cell cycle progression due to ERK knockdown.CONCLUSION Our results indicate that NEK2 plays a carcinogenic role in the malignant proliferation of GC cells via the ERK/MAPK signaling, which may be important for treatment and improving patient survival. | Wei-Dong Fan Tao Chen Peng-Jun Liu | 2019 | World Journal of Gastroenterology2019，25，23： | 7 |
| 20 | Effect of adipose-derived mesenchymal stem cells on hepatocellular carcinoma: In vitro inhibition of carcinogenesis显示文摘AIM To investigate the effect of adipose-derived mesenchymal stem cells(ADMSCs)and their conditioned media(CM) on hepatocellular carcinoma(HCC) cell tumorigenesis.METHODS The proliferation rate of HepG2 and PLC-PRF-5 HCC cancer cells was measured using the trypan blue exclusion method and confirmed using the cell-counting kit8(commonly known as CCK-8) assay. Apoptosis was detected by flow cytometry using annexin V-FITC. Protein and mRNA expression was quantified by ELISA and real time PCR, respectively. Migration and invasion rates were performed by Transwell migration and invasion assays. Wound healing was examined to confirm the data obtained from the migration assays.RESULTS Our data demonstrated that when co-culturing HCC cell lines with ADMSCs or treating them with ADMSC CM, the HCC cell proliferation rate was significantly inhibited and the apoptosis rate increased. The decreased proliferation rate was accompanied by an upregulation of P53 and Retinoblastoma mRNA and a downregulation of c-Myc and hTERT mRNA levels. More notably, ADMSCs and their CM suppressed the expression of the two important markers of HCC carcinogenicity, alpha-fetoprotein and Des-gamma-carboxyprothrombin. In addition, the migration and invasion levels of HepG2 and PLC-PRF-5 cells significantly decreased, potentially through increased expression of the tissue inhibitor metalloproteinases TIMP-1, TIMP-2 and TIMP-3.CONCLUSION These findings shed new light on a protective and therapeutic role for ADMSCs and their CM in controlling HCC invasiveness and carcinogenesis. | Rim Serhal Nagib Saliba George Hilal Mayssam Moussa Ghada S Hassan Oula El Atat Nada Alaaeddine | 2019 | World Journal of Gastroenterology2019，25，5： | 6 |
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