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Table of Content

    05 February 2016, Volume 36 Issue 2
    Role of EGFR in high glucose-induced apoptosis of human renal proximal tubular epithelial cells
    2016, 36(2):  151-155. 
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    Objective To investigate the effect of EGFR signaling pathway in apoptosis of human renal proximal tubular epithelial cells (HK-2) under high concentration of glucose. Methods HK-2 cells were cultured in vitro and divided into 4 groups: normal glucose group, mannitol control group, high glucose group, high glucose plus EGFR inhibitor group. Western blot analysis was used to determine the expression of phosphorylated EGFR, total EGFR, cleaved caspase-3、BAX, BCL-2 and β-actin. MTT assay was used to detect the proliferation of cells. Apoptosis of HK-2 was also analyzed by flow cytometry. Results Compared with normal glucose group and mannitol control group, the number of cell apoptosis (cleaved caspase-3 expression and BAX/BCL-2 ratio), activity of EGFR and endoplasmic reticulum stress (ERS) are significantly increased in HK-2 cells in high glucose group (P<0. 01). Specific EGFR inhibition (AG1478) inhibited high glucose-induced HK-2 cell apoptosis(P<0.05), EGFR activation(P<0.05), endoplasmic reticulum stress(P<0.05). Conclusions Inhibition of EGFR activation may prevent high glucose-induced HK-2 cell apoptosis through decreasing endoplasmic reticulum stress.
    MG132 inhibits TGF-β1-induced activation of human lung fibroblasts
    2016, 36(2):  156-160. 
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    Objective To investigate the effect of ubiquitin-proteasome inhibitor MG132 on TGF-β1-induced activation in lung fibroblasts and its mechanism. Methods The human embryonic lung fibroblasts (MRC-5) were randomly divided into three groups as follows: control group, TGF-β1 group and MG132 group. The protein levels of a-SMA and COL1A1 were detected by Western blot. The mRNA and protein expression of Smad7, SnoN (Ski-related novel gene N), TβRI, Smad2 and Smad3 were detected by RT-PCR and Western blot respectively. Results TGF-β1 treatment of lung fibroblasts increased α-SMA and COL1A1 expression (P <0.05 as compared with control). MG132 inhibited TGF-β1-induced α-SMA and COL1A1 expression in lung fibroblasts (P <0.05 as compared with TGF-β1 group). The mRNA levels of Smad7 and SnoN in TGF-β1 group were increased (P <0.05 as compared with control). The protein levels of Smad7 and SnoN in TGF-β1 group were decreased (P <0.05 as compared with control). Compared with TGF-β1 group, the protein levels of Smad7 and SnoN in MG132 group were increased (P <0.05). Conclusions MG132 could inhibit TGF-β1-induced activation in lung fibroblasts in vitro, which may be associated with the inhibitory effect of MG132 on TGF-β/Smads signaling by preventing degradation of Smad7 and SnoN.
    Cloning of ESRP1 splicing variants and its effects on MDA-MB-231 breast cancer cell line proliferation
    2016, 36(2):  161-166. 
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    Objective To clone ESRP1 splicing variants and construct their lentivirus expression vector. To explore the effects of ESRP1 overexpression on MDA-MB-231 cell proliferation. Methods ESRP1 splicing variants were applified by PCR, in which the OVCAR3 cDNA was used as the template, and then the PCR products of ESRP1 splicing variants were ligated to Myc-tagged pCMV-Myc vector. ESRP1 splicing variants containing Myc-tag were cloned to lentivirus expression vector pLV-tTR/KRAB-Red. These lentivirus expression vectors containing Myc-tagged ESRP1 splicing variants were transfected into 293T cells, and lentivirus were made. MDA-MB-231 cells were infected with lentivirus, the cell proliferation was determined by MTT, and PARP cleavage was examined. Results The lentivirus expression vectors containing Myc-tagged ESRP1 splicing variants were constructed successfully, and the lentivirus were produced. ESRP1 overexpression could inhibit MDA-MB-231 cell proliferation and induce PARP cleavage in MDA-MB-231 cells. Conclusions The lentivirus expression vectors containing Myc-tagged ESRP1 splicing variants were constructed successfully. ESRP1 overexpression could inhibit MDA-MB-231 cell proliferation, and this may be correlated with cell death.
    Ovarian cancer cell promotes the generation of CD8+ regulatory T cells through P38 MAP Kinase signaling
    2016, 36(2):  167-172. 
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    Objective To investigate the effects of mitogen-activated protein kinase (MAPK) signaling pathway on the differentiation of CD8+ regulatory T cells induced by ovarian cancer cell line SKOV3. Methods Coculture systerm of CD8+ T cells and SKOV3 were conducted in vitro, CD8+ T cells cultured alone group acted as control group. At day 5, CD8+ T cells were collected, mRNA and protein expression levels of CD28, CD25, Foxp3 in CD8+ T cells were detected by real-time PCR and flow cytometry, respectively. Western blot was used to detect the expression of p-ERK, ERK, p-JNK,JNK,p-p38MAPK and p38 MAPK. Proliferation assay was applied to analyze the effect of CD8+ T cells on na?ve CD4+ T cells. The phenotypic changes of CD8+T cells were determined after 4 hours pre-incubation with the specific inhibitors of p38 MAPK (SB203580). Results In co-cultured group the mRNA and protein expression levels of CD25 and Foxp3 were higher than those in the control group(P<0.05); and the expression level of CD28 was significantly lower than that in the control group(P<0.05); Result showed that the expression of p-p38 MAPK in the co-cultured group was significant higher than that in the control group (P<0.05); After pre-incubated with SB203580 for 4 hours, the phenotypic of CD8+Tregs was significantly decreased. Conclusions P38 MAP Kinase signaling is required for the generation of CD8+ Tregs induced by ovarian cancer cell, which might be benefit for tumor progression.
    Knocking down Runx3 inhibits BMP9-induced osteogenic differentiation of iMEFs cells
    2016, 36(2):  173-178. 
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    Objective: To analyse knocking down Runx3 on BMP9-induced osteogenic differenciation of iMEFs. Methods:iMEFs were infected with ad-BMP9 and then the expression of endogenous Runx3 was determined by RT-PCR and Western blot. iMEFs were treated with ad-siRunx3 and BMP9,then the alkaline phosphatase( ALP) activity was detected by quantitative and staining assay; calcium deposition was detected by Alizarin Red S staining ; the gene expression levels of Id1,Id2,Id3 and Runx2 were determined by RT-PCR and the protein expression level of DLX5 was determined by western blot. iMEFs were transfected with p(12SBE)- Luc and detected by quantitative. Results BMP9 can inhibit the expression of Runx3.Ad-siRunx3 can inhibit the expression of ALP, which is early osteogenic marker, and the expression of calcium deposition, which is late osteogenic marker . Ad-siRunx3 can inhibit the expression of Id1,Id2, Id3, Runx2 and DLX5 induced by BMP9. Conclusion Knocking down Runx3 can inhibit the BMP9-induced Osteogenic differentiation of iMEFs.
    The effect of SIRT6 on delaying hematopoietic stem cell and progenitor cell senescence with ginsenoside Rg1
    2016, 36(2):  179-185. 
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    Objective To investigate the effect of SIRT6 on delaying hematopoietic stem cell and progenitor cell senescence with ginsenoside Rg1. Methods HSC/HPC aged model in vitro was established by t-BHP to induce Sca-1+ HSC/HPC senescence. HSC/HPC aged model in vivo was established as well through the Sca-1+HSC/HPC serial transplantation. The effect of Rg1 to delay Sca-1+HSC/HPC senencence in vitro as well as in vivo were evaluated by senescence-associated β-galactosidase (SA-β-gal) staining, mixed hematopoietic progenitor cell culture(CFU-Mix) and cell cycle assay. The expressions of SIRT6 mRNA and protein were detected by quantitative PCR and Western blotting. Results Compared with aged model in vitro and in vivo, the number of cells entered G0/G1 phase and the percentage of SA-β-gal positive cells were decreased, the number of CFU-Mix was increased in Rg1 treated group and Rg1 prevented group. The expression of SIRT6 mRNA and protein were up regulated in Rg1 treated group and Rg1 prevented group, compared with aged model. The changes of Rg1 prevented group was significantly higher than Rg1 treated group. Conclusion Rg1 could delay Sca-1+HSC/HPC senescence in vitro and in vivo via regulating the expression of SIRT6.
    Characterization of the binding property and the identification of the interaction proteins of GIPC2 PDZ domain by validation screening of PDZ ligand library
    2016, 36(2):  186-190. 
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    Objective To characterize the binding property of GIPC2 PDZ domain by validation screening of PDZ ligand library, and identification of the interaction proteins of GIPC2. Methods 1) The binding properties of GIPC2 PDZ domain were characterized by validation screening of the PDZ ligand library with yeast two-hybrid approach, 2) According to the subcellular localization, involvement in the development of tumor, combined with the PDZ binding properties, the candidate GIPC2 binding ligands were predicted. 3) The candidate ligands were validated with GIPC2 PDZ domain and GIPC2. Results 1) The binding property of GIPC2 PDZ domain is that the last four amino acid residues of C termini are –X-S/T-X-V/L/I and belonging a type I PDZ ligand. 2) Integrated the biological characterization of GIPC2 and the PDZ binding properties, 47 candidate GIPC2 binding ligands were predicted. 3) 10 of 47 candidate ligands were validated to interact with GIPC2 PDZ domain and GIPC2 using yeast two hybrid. Conclusions Ten interaction proteins of GIPC2 were identified.
    Effect of specific integrin-linked kinase siRNA on EMT of human EJ bladder cancer cells and growth of transplanted bladder cancer
    2016, 36(2):  191-198. 
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    Objective To investigate the effect of specific integrin-linked kinase siRNA on proliferation and metastasis of human EJ bladder cancer cells and growth of transplanted bladder cancer. Methods Specific ILK siRNA plasmid and negative control plasmid were stably transfected into bladder cancer EJ cells.Then the effect of ILK siRNA on cytoskeleton was observed under laser confocal microscope.The expression of p-AKT,p-GSK-3β was evaluated by Western Blot.And the expression of p-AKT,p-GSK-3β of transfected cells was detected by immunofluorescence staining. RI co-localized with ILK in EJ cells by immunofluorescence experiments.The EJ cells was determined for proliferative activity by MTT and the distribution of cell cycle by flow cytometry.EJ cells stably expressing ILK siRNA were injected into nude mice.Morphology of tumor and lung tissue was observed with H&E staining.The expression of ILK,RI,NM23-H1 and E-Cadherin in tumor tissue was detected by immunohistochemistry. The change of p-AKT,p-GSK-3β and CD31 of transplanted bladder cancer was determined by immunofluorescence. Results ILK siRNA can inhibit the movement of EJ cells. Compared with control,EJ siRNA cells obviously decreased the expression of p-AKT,p-GSK-3β(P<0.05). The specific ILK siRNA can weaken the proliferating ability of EJ cells.ILK siRNA can inhibit the growth and metastasis of transplanted bladder cancer in nude mice. Conclusion The siRNA plasmid for ILK gene can inhibit EMT and decrease proliferation and metastasis ability significantly in EJ cells.
    Effects of up-regulating RI on EMT and metastasis of mouse melanoma B16-F10
    2016, 36(2):  199-206. 
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    Objective To investigate the effects of ribonuclease inhibitor expression on EMT and metastasis of mouse melanoma B16-F10 cells. Methods RI eukaryotic expression plasmid pIRES2-EGFP-RI was constructed, then transfected into B16-F10 cells, RI expression was identified by RT-PCR, Western blot and immunofluorescence assay. Cell morphology was observed by HE staining and phase contrast microscope. The cytoskeleton change was detected with FITC phalloidin staining under laser scanning confocal microscope. The adhesion assay, scratch assay and Transwell assay were used to detect the cell adhesion, migration and invasion ability. The expressions of metastasis and EMT related proteins were determined by Western blot. Various B16-F10 cells were respectively injected into the vein of the eye socket of c57/BL mice to establish pulmonary metastasis animal model. Three weeks after injection, the mice were sacrificed, lungs were removed and weighed. And then the number of metastasis nodules was counted under a dissecting microscope. The lung tissue sections were stained with HE staining, and the expressions of metastasis and EMT related proteins were detected by immunohistochemistry.Results The results showed that up-regulation of RI inhibited migration and invasion as well as changed cell morphology, adhesion and rearranged cytoskeleton in vitro. In addition, the data indicated that over-expression RI induced up-regulation of E-cadherin, accompanied with decreased expressions of proteins associated with EMT such as N-cadherin, snail, slug, vimentin and twist both in vitro and in vivo. Furthermore, RI restrained matrix metalloproteinase MMP-2 and MMP -9 secretions in B16-F10 melanoma cells. Finally, the data showed that RI suppressed invasiveness and metastasis by the experimental metastasis models of melanoma with lighter lung weight, a fewer metastasis nodules and a lower incidence rate, with respect to the control groups. Conclusion Up-regulating ribonuclease inhibitor could significantly inhibit EMT, invasion and metastasis of B16-F10 cell. These results suggest that RI could be a therapeutic target protein for melanoma.
    Effects of miR-760 on cell proliferation, migration and invasion of gastric cancer cell lines MGC-803
    Fang WANG Ai-Hua Liang
    2016, 36(2):  207-210. 
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    Objective To investigate the effects of miR-760 on cell proliferation, migration and invasion of gastric cancer cell line MGC-803. Methods The level of miR-760 expression was detected by real-time RT-PCR in 50 paired gastric cancer tissues and their adjacent normal tissues. miR-760 overexpression was achieved by transfection of construct pcDNA-miR-760 into MGC-803 cells. The proliferation, migration and invasion of MGC-803 cells were detected by the CCK-8, Transwell and scratch wound assay, respectively. Results miR-760 was decreased in 36 cases (72%) of gastric cancer tissues compared to their control. Furthermore, overexpression of miR-760 effectively inhibited the migration and invasion of MGC-803 cells(p<0.05), but had no effects on proliferation. Conclusion Down-regulation of miR-760 has a correlation with the progression of gastric cancer. Up-regulation of miR-760 can inhibit the invasion and migration of MGC-803 cells.
    Effect and mechanism of all-trans retinoic acid on proliferation, migration, and invasion of mouse hepatocellular carcinoma cell line Hepa1-6
    2016, 36(2):  211-217. 
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    Objective To observe the effect of all-trans retinoic acid (ATRA) on the proliferation, apoptosis, migration and invasion of hepatocellular carcinoma cell line Hepa1-6 cell and investigate the mRNA expression of mesenchymal markers and microRNAs. Methods The Hepa1-6 cells were treated with DMEM containing different concentrations of ATRA (0, 0.1, 1.0, 10.0 μmol/L). Trypan blue and Crystal Violet Staining were used to assess cell proliferation at indicated time points. The apoptosis was examined by Hoechst Staining. Migration and invasion abilities of cells were detected by Wound Healing assay and Transwell assay, respectively. The mRNA expression of mesenchymal markers (N-cadherin, sail, vimentin) of Hepa1-6 with ATRA at different concentrations and miRNA200s with10.0 μmol/L ATRA treatment were detected by real-time PCR. Results Compared with control group (0 μmol/L), after treatment with ATRA, the proliferation, migration and invasion capacity of Hepa1-6 cells were obviously inhibited (P<0.05), and the apoptosis rates increased significantly. The mRNA expression of mesenchymal markers (N-cadherin, sail, vimentin) was decreased. Furthermore, the role of ATRA on these was strengthened with the increased concentrations of ATRA treatment. In addition, miR200a-3p, miR200c-3p, miR141-3p were up-regulated. Conclusion ATRA can inhibit the growth, migration, invasion and down-regulate mesenchymal markers (N-cadherin, sail, vimentin) of hepatocellular carcinoma cell line Hepa1-6 cell, induce its apoptosis in a concentration-dependent manner. These may be related to the up-regulation of miR200s and inhibition of mesenchymal phenotypes.
    High resolution melting applied to the mutation identification in a family with Wilson’s disease
    2016, 36(2):  218-221. 
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    Objective To identify the ATP7B mutation and perform the prenatal gene diagnosis in a family with Wilson’s disease(WD). Methods Genomic DNA was extracted from the peripheral blood and the fetal villi tissue by standard phenol/chloroform method. PCR and Sanger DNA sequencing was used to analyze the causative mutation in the proband; Mutation identification was performed in the other 4 familial members including a fetus with high risk of WD by PCR-HRM. In the same way, a prenatal gene diagnosis was completed successfully in the mother of the proband. DNA sequencing was used to validate the genotype of the samples in different HRM-curves. Results Genetic sequencing showed that the proband was a homozygote of the missense mutation c.2333G>T (p.R778L) , which was located in the exon 8 of gene ATP7B. HRM analysis displayed three different curves, representing three different genotypes. The curve types for the 5 familial members and 4 normal control samples were consistent with genetic sequencing: the proband himself was a mutant homozygote, all the other family members were the heterozygote of the mutation, and the 4 normal controls were wild type. Conclusions The authors found a known mutation of p.R778L in a WD family, and the prenatal gene diagnosis was achieved in a fetus with high risk by PCR-HRM.
    Expression and correlation of human herpes viruses 6 and vascular endothelial growth factor C in oral squamous carcinoma
    2016, 36(2):  222-226. 
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    OBJECTIVE: Detect the mRNA and the proteins expression of human herpes viruses 6 (HHV-6) and vascular endothelial growth factor C(VEGF-C) in normal oral tissues and oral squamous cell carcinomas, To investigate the relationship between the expression levels and the development of oral squamous cell carcinomas. Moreover, discuss the correlation of HHV-6 infection and expression levels of VEGF-C. METHODS: The expression levels of HHV-6 and VEGF-C mRNA in oral squamous cell carcinomas were quantified by real-time PCR, as well as the protein levels were evaluated by immunohistochemistry. RESULTS: The expression levels of HHV-6 and VEGF-C mRNA in oral squamous cell carcinomas were significantly higher than normal oral tissues, so does their protein (P<0.05).The mRNA expression levels have a significant positive correlation between HHV-6 and VEGF-C in the same oral squamous cell carcinomas ( P<0.001). The expression levels of HHV-6 and VEGF-C in the oral squamous cell carcinomas has significantly correlation with lymph node metastasis(P<0.05). CONCLUSION: The occurrence of oral squamous carcinoma is associated with the infection of HHV-6, and it’s infection may cause the high expression of VEGF-C.
    The expression difference of ADAM15,MMP-2 and MMP-9 in different breast cancer cell lines
    2016, 36(2):  227-231. 
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    Objective Explore the expression of ADAM15、MMP-2 and MMP-9 in different breast cancer cell lines through experiment to investigate the relativity of the metastasis of breast cancer cell.Methods Transwell chamber experiments were used to test the metastasis of two breast cancer cell lines.Immunocytochemical were used to carry out qualitative analysis,localization and semi-quantitative detection and quantitative detection through Western blot for ADAM15、MMP-2 and MMP-9.Results The migration of MDA-MB-231 breast cancer cell line is stronger than the MCF-7,s.The expression of ADAM15、MMP-2 and MMP-9 in the MDA-MB-231 breast cancer cell line are higher than that in the MCF-7(immunohistochemistry:P<0.001,P<0.05,P<0.001;Western blot:P<0.01,P<0.05,P<0.01),and the difference of ADAM15 is more obvious than MMP-9 and MMP2 in two cell lines .Conclusion The expression of ADAM15、MMP-2 and MMP-9 closely correlate to the metastasis of breast cancer cells,and infer that ADAM15 may have a closer relationship to the metastasis of breast cancer cells than the others.
    H2S inhibits resistin secretion in mouse insulin-resistant 3T3-L1 adipocytes
    2016, 36(2):  232-236. 
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    Objective To investigate whether H2S can inhibit resistin secretion in mouse insulin-resistant 3T3-L1 adipocytes via activation of amp-activated protein kinase. Methods The cells were divided into the normal groups, the insulin resistance groups and the 50 umol/L NaHS treatmen tgroups. The ELISA method was used to analyze the level of resistin secretion, Western blot was used to analyze the expression of activated protein kinase (AMPK) and acetyl coenzyme A carboxylase enzyme (ACC) phosphorylation protein and RT-PCR was performed to analyzed the expression of resistin mRNA and AMPK mRNA. Results The effects of NaHS significantly decreased the secretion level of resistin compared with the control group(P<0.05). The expression of AMPK and ACC protein phosphorylation in normal and insulin resistant cells significantly increased(P<0.05). The AMPK pathway inhibitor compound C markly weakened the effects on AMPK and ACC protein phosphorylation. At the same time, the secretion level of resistin was inhibited. Conclusion Hydrogen sulflide may inhibits resistin secretion in mouse insulin-resistant 3T3-L1 adipocytes via activation of AMP-activated protein kinase.
    Proliferation inhibition of Tca8113 cell induced by cinnamic acid
    2016, 36(2):  237-242. 
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    Objective To investigate the effect of cinnamic acid on the proliferation of tongue squamous cell carcinoma cell line Tca8113. Methods After treated with cinnamie acid,the morphological changes of Tca8113 were observed under inverted microscope. The proliferation inhibition of Tca8113 cell was detected by MTT method. The cell cycle of Tca8113 was analyzed by flow cytometry. The protein levels of KLF6,Bcl-2,p53,cyclin D1,c-Jun and PTEN were measured by the method of immunohistochemistry. Results It was showed that the proliferation of Tca8113 cells can be inhibited significantly by cinnnamic acid in vitro(p<0.05) ,and the inhibition is time and dose dependent; Typical feature of induced differentiation of Tca8113 cells was observed. After treated with cinnamic acid,the cell number in G1 and G2 phase was decreased significantly while the number in S phase was increased significantly.Tca8113 cells were significantly arrested in S phase (p<0.05) . The protein levels of KLF6 and p53 were increased(p<0.05) whereas the protein levels of Bcl-2, cyclin D1 and c-Jun decreased significantly(p<0.05). Conclusion Cinnamic acid inhibits the proliferation of Tca8113 cell by arresting the cell cycle in S phase,and then may induce TCA 8113 cell to apoptosis finally.
    Clinical features of systemic lupus erythematosus complicated with thymoma
    2016, 36(2):  243-247. 
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    Objective To investigate the clinical characteristics of systemic lupus erythematosus (SLE) with thymoma. Methods The clinical manifestations, laboratory tests, treatment and prognosis of SLE with thymoma from 1984 to 2015 in Peking Union Medical College Hospital were retrospectively reviewed. And comparison of cases in our study and in the literature was made. Results 11 cases of SLE patients complicated with thymoma were collected. The prevalence of thymoma in the total SLE patients was 1.55‰ and the prevalence of SLE in the total thymoma patients was 1.07% during the same period. 10 were female and 1 was man. The mean ages of the onset and diagnosis of SLE were 25.5 and 26.4 years old respectively. The mean age of thymoma was 28.5 years old. The average disease course from SLE to thymoma was 2.1 years old. The mean SLEDAI at the diagnosis of thymoma complicated with SLE was 3.6. 5 patients were performed thymectomy and 1 patient was given radiotherapy. According to the WHO classifications of thymoma, 2 cases were type A, 1 case was type AB, and 1 case was type C. 8 patients were followed up for 3 to 92 months, including 6 patients SLE stable, 1 patient SLE flare and 1 patient died of tumor metastasis. Compared with cases in the literature, our patients were younger and the rate of thymectomy was lower. Conclusions The coincidence of thymoma and SLE was not rare. Thymoma was concealed and could be involved in the pathogenesis of SLE. Thymectomy might contribute to the remission of SLE, which should arise the attention of clinicians.
    Research progress of virus infection in the asthma exacerbation
    2016, 36(2):  253-257. 
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    The airway inflammation is the nature of asthma. Although symptoms can be well controlled by corticosteroids andβ2-agonists, viral respiratory tract infections can still cause exacerbations. The defect of inherent and adaptive immunity impaired the the antiviral response, with the synergetic effect of allergic inflammatory reaction. The better understanding of the mechanism will provide new prevention and treatment of the disease.
    Advances in research on Neuropilin-1
    2016, 36(2):  258-261. 
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    Neuropilin-1(NRP1) is an important member of the NRP-family, which plays an important role in neural development, angiogenesis, tumor metastasis and immunity as NRP1 in various fields. NRP1 can promote tumor angiogenesis, proliferation and metastasis through a variety of mechanisms, while in the immune system it can regulate the primary immune response and which is a key factor in anti-tumor immunity. Further research of NRP1 will provide new directions and opportunities for the nervous system, vascular system and tumor treatment.
    Research progress of CPT1 gene in tumor
    2016, 36(2):  262-266. 
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    Carnitine palmitoyltransferase 1 (CPT1) is the key and rate-limiting enzyme of long chain fatty acids β-oxidation in liver cells. CPT1A and CPT1C are subtypes of CPT1 which can promote tumor growth. CPT1A was overexpressed and amplificated in glioblastoma, lymphoma, esophageal cancer and breast cancer. The drugs which could inhibit the activity or expression of CPT1A had anti-tumor effects. Therefore, CPT1 has roles in promoting the tumorigenesis, and it may develop into an molecular biomarker and a new target for cancer therapy.
    The influence of interaction between lncRNA and miRNA on disease
    Hong YI 易红
    2016, 36(2):  267-271. 
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    There is a interaction between long con-coding RNA(lncRNA) and microRNA(miRNA). lncRNA can interact with the miRNA as a competing endogenous RNA(ceRNA) to participate in the expression regulation of target genes. Whereas miRNA can regulate lncRNA to exert biological functions by RNA-inducde silencing complex(RISC). The interaction between lncRNA and miRNA participates in the occurrence of various diseases together. Now this paper summarizes the influence of interaction between lncRNA and miRNA on disease.
    Transcription factor-driven EMT in cancer invasion and metastasis
    2016, 36(2):  272-276. 
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    Epithelial-mesenchymal transition (EMT) is regarded as a key step in cancer invasion and metastasis. Transcriptional factors (TFs) are the primary clues in initiating EMT, such as SNAIL, TWIST and ZEB. TFs modulate transcription of EMT-associated genes. Meanwhile, they also experienced epigenetic reprogramming and transcriptional and post-transcriptional regulation. Elucidation the molecular mechanisms of TF-driven EMT in cancer invasion and metastasis would provide new insights in target therapy and drug design.
    Recent advances in the study of pluripotent stem cell generation
    2016, 36(2):  277-280. 
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    Pluripotent stem cells provide an ideal cell source for the study of the molecular mechanisms of disease, drug screening and regenerative medicine applications, however, the current study of pluripotent stem cells is facing many bottlenecks and challenges in generation. To provide ideas for further study, here, we review recent advances in the study of pluripotent stem cell generation.
    Research progress of microRNAs in prostate cancer
    2016, 36(2):  281-284. 
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    Prostate cancer(PCa) is a common malignant tumor of urinary tract in males. MicroRNAs (miRNAs) modulate expression of target genes, which involved in the regulation of tumorigenes, invasion and metastasis process. In recent studies, many miRNAs play a role of oncogenes or tumor suppressor genes,which regulate cell proliferation, apoptosis, invasion and migration.
    Exploration in the adhibition of the simulation model in obstetrics and gynecology
    2016, 36(2):  285-288. 
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    Based on the medical treatment status in China, problems of medical education have become more prominent. Owing to the particularity of obstetrics and Gynecology, clinical teaching is more difficult. Introducing of the simulation model would not only reduce the difficulty of teaching of obstetrics and gynecology, but also inaugurate new paths for the teaching of obstetrics and gynecology. The author analyzed and summarized the adhibition, advantages and disadvantages of the simulation model in the education of obstetrics and gynecology, and then explored the method of the improvement.