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Influence of irbesartan on expression of ILK and its relationship with epithelial-mesenchymal transition in mice with unilateral ureteral obstruction

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Acta Pharmacologica Sinica 2007年第11期28卷 1810-1818页

作者： Bi-cheng LIU~1,Hui-ling XIA,Ji-ning WU,Xiao-liang ZHANG,Dian-ge LIU,Yu-xiang GONGInstitute of Nephrology,Zhong Da Hospital,Southeast University.Nanjing 210009,China Institute of Nephrology Zhong Da Hospital Southeast University Nanjing China

Aim:Irbesartan,a new antagonist of the type Ⅰ angiotensin Ⅱ receptor,has beenproven to be renal protective in both diabetic and non-diabetic nephropathy,butits exact mechanism is still *** we investigated the influence ofirbesartan on the expression of the integrin-linked kinase (ILK) and its relation-ship with epithelial-mesenchymal transition (EMT) in mice with unilateral ureteralobstruction (UUO).Methods:The mice were randomly divided into 3 groups:sham operation (C,n=20),UUO (n=40),and UUO with irbesartan treatment(UUO+irbesartan,n=40).Irbesartan was given at a dose of 50 mg/kg body weightper day by *** experimental animals in the control group received thesame volume of vehicle (0.9% saline solution).The animals were sacrificed at d 1,3,7,and 14,respectively,after the ***:The expression of the ILK atmRNA and protein levels were significantly increased in the UUO group 1 d afterthe surgery,which was significantly decreased by treatment with irbesartan (P<0.01,respectively).The expression of α-smooth muscle actin (α-SMA) was sig-nificantly increased,while E-cadherin was decreased in mice with UUO at d 3 afterthe *** with irbesartan significantly abrogated such effects (P<0.01).The immunohistochemistry analysis indicated that the protein expressionof the ILK was positively correlated with α-SMA,but negatively with ***:These results suggested that irbesartan attenuated renaltubulointerstitial fibrosis in UUO mice,which may be related to the inhibition ofILK expression,subsequently preventing the tubular EMT.

关键词： irbesartan integrin-linked kinase epithelialmesenchymal transition tubulointerstitial fibrosis

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Effects of epidermal growth factor on transforming growth factor-beta1-induced epithelial-mesenchymal transition and potential mechanism in human corneal epithelial cells

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International Journal of Ophthalmology(English edition) 2020年第1期13卷 11-20页

作者： Shu-Yang Chen Chen Xie Hong Zhu Ye Shen Department of Ophthalmology First Affiliated HospitalCollege of MedicineZhejiang UniversityHangzhou 310003Zhejiang ProvinceChina Tongde Hospital of Zhejiang Province Hangzhou 310012Zhejiang ProvinceChina Clinical Research Center the First Affiliate HospitalSchool of MedicineZhejiang UniversityHangzhou 310003Zhejiang ProvinceChina

AIM: To evaluate the effects of epidermal growth factor(EGF) on transforming growth factor-beta1(TGF-β1)-induced epithelial-mesenchymal transition(EMT) in human corneal epithelial cells(HCECs). METHODS: HCECs were cultured and treated with TGF-β1 for establishing the model of EMT in vitro. Biological effect of EGF on TGF-β1-induced EMT was evaluated. Proteins and m RNAs expression changes of E-cadherin, N-cadherin and Fibronectin(EMT-relative markers) after TGF-β1 or TGF-β1 combined EGF treatment were detected by Western blot and RT-PCR, respectively. Viability and migration of HCECs were measured by CCK-8, transwell cell migration assay and cell scratch wound healing assay. Activation of Smad2, ERK, p38, JNK and Akt signaling pathways were evaluated by Western blot. Inhibitors of relevant signaling pathways were added to the HCECs to explore the key signal ***: With treatment of TGF-β1 only, three EMTrelative proteins and m RNA expression showed that EMT up-regulated in a concentration-dependent and time-dependent manner, with significantly decreasing cell viability(TGF-β1≥5 ng/m L, P<0.05) and increasing cell migration(TGF-β1≥5 ng/m L, P<0.01). The phosphorylation of Smad2 and p38 was a key process of TGF-β1-induced EMT. Meanwhile, EMT-relative proteins and m RNA expression showed that EGF inhibited TGF-β1-indued EMT, with significantly increasing cell viability(EGF≥10 ng/m L, P<0.01). It was noteworthy that EGF significantly enhanced cell migration although EMT was inhibited(EGF≥10 ng/m L, P<0.01), and the blockage of p38(by SB202190, a p38 inhibitor) was a potential mechanism of this phenomenon. CONCLUSION: EGF inhibits TGF-β1-induced EMT via suppressive p38, and promotes cells proliferation and migration in a non-EMT process by inhibiting p38 pathway.

关键词： epidermal growth factor p38 epithelialmesenchymal transition corneal epithelial cell

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Bone morphogenetic protein-6 suppresses TGF-β_(2)-induced epithelial-mesenchymal transition in retinal pigment epithelium

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International Journal of Ophthalmology(English edition) 2024年第4期17卷 646-652页

作者： Xuan Liu Ming Liu Meng Ji Bo Ma Yu-Cen Hou Xin-Yue Yao Qiao-Chu Cheng Li Chen Department of Ophthalmology the First Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710061Shaanxi ProvinceChina Department of Ophthalmology Xi’an No.1 HospitalXi’an 710000Shaanxi ProvinceChina Shaanxi Institute of Ophthalmology Xi’an 710000Shaanxi ProvinceChina Department of Ophthalmology Ankang Hospital of Traditional Chinese MedicineAnkang 725000Shaanxi ProvinceChina

AIM:To evaluate the effect of bone morphogenetic protein-6(BMP-6)on transforming growth factor(TGF)-β_(2)-induced epithelial-mesenchymal transition(EMT)in retinal pigment epithelium(RPE).METHODS:Adult retinal pigment epithelial cell line(ARPE-19)were randomly divided into control,TGF-β_(2)(5μg/L),and BMP-6 small interfering RNA(siRNA)*** cell morphology was observed by microscopy,and the cell migration ability were detected by Transwell *** EMT-related indexes and BMP-6 protein levels were detected by Western ***,a BMP-6 overexpression plasmid was constructed and RPE cells were divided into the control group,TGF-β_(2)+empty plasmid group,BMP-6 overexpression group,and TGF-β_(2)+BMP-6 overexpression *** EMT-related indexes and extracellular regulated protein kinases(ERK)protein levels were ***:Compared with the control group,the migration of RPE cells in the TGF-β_(2) group was significantly ***-β_(2) increased the protein expression levels ofα-smooth muscle actin(α-SMA),fibronectin and vimentin but significantly decreased the protein levels of E-cadherin and BMP-6(P<0.05)in ***,the migration of RPE cells in the BMP-6 siRNA group was also significantly ***-6 siRNA increased the protein expression levels ofα-SMA,fibronectin and vimentin but significantly decreased the protein expression levels of E-cadherin(P<0.05).Overexpression of BMP-6 inhibited the migration of RPE cells induced by TGF-β_(2) and prevented TGF-β_(2) from affecting EMT-related biomarkers(P<0.05).CONCLUSION:BMP-6 prevents the EMT in RPE cells induced by TGF-β_(2),which may provide a theoretical basis for the prevention and treatment of proliferative vitreoretinopathy.

关键词： bone morphogenetic protein-6 epithelialmesenchymal transition transforming growth factor-β_(2) retinal pigment epithelial cells cell migration

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Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis

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Genes & Diseases 2020年第2期7卷 172-184页

作者： Yifan Wang Chenfang Dong Binhua P.Zhou Cancer Institute of Integrative Medicine Zhejiang Academy of Traditional Chinese MedicineHangzhouZhejiang310012China Department of Pathology and Pathophysiology Department of Surgical Oncology(Breast Center)of the Second Affiliated HospitalZhejiang University School of MedicineHangzhou310058China Departments of Molecular and Cellular Biochemistry Markey Cancer CenterUniversity of Kentucky School of MedicineLexingtonKY40506USA

Epithelial-mesenchymal transition(EMT)is a de-differentiation program that imparts tumor cells with the phenotypic and cellular plasticity required for drug resistance,metastasis,and *** dynamic and reversible events is governed by a network of EMT-transcription factors(EMT-TFs)through epigenetic *** chromatin modifying-enzymes utilize metabolic intermediates as cofactors or substrates;this suggests that EMT is subjected to the metabolic ***,EMT rewires metabolic program to accommodate cellular changes during *** we summarize the latest findings regarding the epigenetic regulation of EMT,and discuss the mutual interactions among metabolism,epigenetic regulation,and ***,we provide perspectives of how this interplay contributes to cellular plasticity,which may result in the clinical manifestation of tumor heterogeneity.

关键词： Epigenetics epithelialmesenchymal transition Heterogeneity Metabolism Plasticity

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Adenomyosis-derived extracellular vesicles endow endometrial epithelial cells with an invasive phenotype through epithelial-mesenchymal transition

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Genes & Diseases 2020年第4期7卷 636-648页

作者： Dayong Chen Hai Qiao Yiting Wang Ling Zhou Na Yin Liaoqiong Fang Zhibiao Wang State Key Laboratory of Ultrasound Engineering in Medicine Co-Founded by Chongqing and the Ministry of Science and Technology College of Biomedical EngineeringChongqing Key Laboratory of Biomedical EngineeringChongqing Medical University40016PR China

Extracellular vesicles from highly metastatic tumor cells have been shown to mediate epithelial-mesenchymal transition(EMT)-related events in recipient *** endometrial epithelial cells,EMT processes are known to be involved in the development of *** aimed to investigate whether adenomyosis-derived extracellular vesicles(AMEVs)are able to induce an EMT process in endometrial epithelial *** this study,AMEVs were isolated from patients with adenomyosis and characterized by transmission electron microscopy,Western blot,and nanoparticle *** endometrial epithelial cells(EECs)were derived from normal endometrium tissues from patients with leiomyoma and co-cultured with AMEVs in *** uptake was examined by fluorescence confocal *** invasion of EECs was confirmed by Transwell ***,Western blot,and qRT-PCR were performed on EECs to illustrate the expression levels of cytokeratin 19,E-cadherin,vimentin,and zinc finger E-boxbinding homeobox 1(ZEB1).The results indicated that the cellular fluorescence intensity gradually increased after 48 h of co-culture,but decreased after 72 *** co-culturing with AMEVs for 72 h,EECs expressed significantly lower levels of cytokeratin 19 and E-cadherin,and significantly higher levels of vimentin and *** these results demonstrated that AMEVs induce an EMT process and enhance the invasion of *** changes may contribute to the pathogenesis and progression of adenomyosis.

关键词： Adenomyosis epithelialmesenchymal transition Extracellular vesicles Primary endometrial epithelial cells Pathogenesis

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Correction to “Interleukin-34 promotes the proliferation and epithelial-mesenchymal transition of gastric cancer cells”

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World Journal of Gastrointestinal Oncology 2023年第9期15卷 1673-1674页

作者： Chuan-Hong Li Zhang-Ming Chen Pei-Feng Chen Lei Meng Wan-Nian Sui Song-Cheng Ying A-Man Xu Wen-Xiu Han Department of General Surgery First Affiliated Hospital of Anhui Medical UniversityHefei 230022Anhui ProvinceChina Department of Immunology College of Basic MedicineAnhui Medical UniversityHefei 230022Anhui ProvinceChina

Correction to“Interleukin-34 promotes the proliferation and epithelialmesenchymal transition of gastric cancer cells”.In this article,we found the following error in Figure 3A:The panel image"24 h,sh-RNA1"in the AGS cells wound healing assay was incorrectly inserted during the preparation of the submission;the correct figure is provided in this correction.

关键词： Correction Gastric cancer Interleukin-34 Proliferation epithelialmesenchymal transition Metastasis

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BMSC-derived Exosomes Ameliorate Peritoneal Dialysis-associated Peritoneal Fibrosis via the Mir-27a-3p/TP53 Pathway

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Current Medical Science 2024年第2期44卷 333-345页

作者： Jun-li ZHAO Lin ZHAO Qiu-nan ZHAN Miao LIU Ting ZHANG Wen-wen CHU Department of Nephrology Shanghai University of Medicine&Health Sciences Affiliated Zhoupu HospitalShanghai 201318China Orthopedic Department Guangming Traditional Chinese Medicine Hospital of Pudong New AreaShanghai 201399China

Objective:Peritoneal fibrosis(PF)is the main cause of declining efficiency and ultrafiltration failure of the peritoneum,which restricts the long-term application of peritoneal dialysis(PD).This study aimed to investigate the therapeutic effects and mechanisms of bone marrow mesenchymal stem cells-derived exosomes(BMSC-Exos)on PF in response to ***:Small RNA sequencing analysis of BMSC-Exos was performed by second-generation sequencing.C57BL/6J mice were infused with 4.25%glucose-based peritoneal dialysis fluid(PDF)for 6 consecutive weeks to establish a PF model.A total of 36 mice were randomly divided into 6 groups:control group,1.5%PDF group,2.5%PDF group,4.25%PDF group,BMSC-Exos treatment group,and BMSC-Exos+TP53 treatment *** transcription quantitative polymerase chain reaction(RT-qPCR)was performed to measure the expression level of miR-27a-3p in BMSC-Exos and peritoneum of mice treated with different concentrations of *** and Masson staining were performed to evaluate the extent of *** therapeutic potential of BMSC-Exos for PF was examined through pathological examination,RT-qPCR,Western blotting,and peritoneal function ***-mesenchymal transition(EMT)of HMrSV5 was induced with 4.25%*** were divided into control group,4.25%PDF group,BMSC-Exos treatment group,and BMSC-Exos+TP53 treatment *** Counting Kit-8 assay was used to measure cell viability,and transwell migration assay was used to verify the capacity of BMSC-Exos to inhibit EMT in HMrSV5 ***:Small RNA sequencing analysis showed that miR-27a-3p was highly expressed in BMSC-derived exosomes compared to *** RT-qPCR results showed that the expression of miR-27a-3p was upregulated in BMSC-Exos,but decreased in PD *** found that PF was glucose concentration-dependently enhanced in the peritoneum of the PD *** with the control mice,the PD mice showed high solute transport and decreased ultrafiltration volume as well as an obvious f

关键词： peritoneal fibrosis bone marrow mesenchymal stem cell-derived exosomes miR-27a-3p TP53 epithelialmesenchymal transition

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Inhibition of bromodomain-containing protein 4 enhances the migration of esophageal squamous cell carcinoma cells by inducing cell autophagy

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World Journal of Gastrointestinal Oncology 2022年第12期14卷 2340-2352页

作者： Wen-Qian Yang Rui Liang Man-Qi Gao Yu-Zhen Liu Bo Qi Bao-Sheng Zhao Department of Thoracic Surgery The First Affiliated Hospital of Xinxiang Medical UniversityWeihui 453100Henan ProvinceChina Esophageal Cancer Institute Xinxiang Medical UniversityWeihui 453100Henan ProvinceChina Life Science Research Center The First Affiliated Hospital of Xinxiang Medical UniversityWeihui 453100Henan ProvinceChina

BACKGROUND Esophageal squamous cell carcinoma(ESCC),the predominant type of esophageal cancer,has a 5-year survival rate less than 20%.Although the cause of poor prognosis is the high incidence and mortality of ESCC,the high rate of metastasis after esophageal cancer surgery is the main cause of death after the ***-containing protein 4(BRD4),an epigenetic reader of chromatinacetylated histones in tumorigenesis and development,plays an essential role in regulating oncogene ***4 inhibition and BRD4 inhibition-based treatment can potentially suppress ESCC ***,the effects and mechanisms of action of BRD4 on ESCC cell migration remain *** To explore the effect of BRD4 on cell migration of ESCC in vitro and its possible molecular *** Human ESCC cell lines KYSE-450 and KYSE-150 were *** 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay was performed to examine cell proliferation,and the transwell migration assay was conducted to test ESCC cell ***1,a BRD4 inhibitor,was applied to cells,and BRD4 siRNA was transfected into ESCC cells to knockdown endogenous ***-RFP-LC3 adenovirus was infected into ESCC cells to evaluate the effect of JQ1 on *** blotting was performed to determine the protein levels of BRD4,E-cadherin,vimentin,AMP-activated protein kinase(AMPK),and *** BRD4 was either downregulated by small interfering RNA or pretreated with JQ1 in ESCC cells,leading to increased tumor migration in ESCC cells in a dose-and time-dependent *** of BRD4 not only significantly suppressed cell proliferation but also strongly increased cell migration by inducing epithelial-mesenchymal transition(EMT).The protein expression of vimentin was increased and E-cadherin decreased in a dose-dependent manner,subsequently promoting autophagy in KYSE-450 and KYSE-150 *** with JQ1,a BRD4 inhibitor,inhibited BRD4-induced LC3-II activation and

关键词： JQ1 Bromodomain-containing protein 4 Cell migration Cell autophagy epithelialmesenchymal transition Esophageal squamous cell carcinoma

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LncRNA cancer susceptibility 20 regulates the metastasis of human gastric cancer cells via the miR-143-5p/MEMO1 molecular axis

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World Journal of Gastroenterology 2022年第16期28卷 1656-1670页

作者： Ke-Shu Shan Wei-Wei Li Wang Ren Shuai Kong Li-Pan Peng Hong-Qing Zhuo Shu-Bo Tian Department of Gastrointestinal Surgery Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250021Shandong ProvinceChina Department of Gastrointestinal Surgery Shandong Provincial Hospital Affiliated to Shandong UniversityJinan 250021Shandong ProvinceChina Department of Critical Care Medicine The 960^(th)Hospital of the People's Liberation Army Joint Logistics Support ForceJinan 250031Shandong ProvinceChina Department of General Surgery People's Hospital of Sishui CountyJining 273200Shandong ProvinceChina

BACKGROUND Gastric cancer(GC)is considered as one of the most widespread *** evidence has shown that lncRNAs can function as important oncogenes or tumor suppressors during GC *** To investigate the effect and mechanism of lncRNA cancer susceptibility 20(CASC20)in the proliferation and metastasis of GC *** Data mining and clinical samples were used to evaluate the expression of CASC20 in GC and adjacent ***20 was down-regulated in GC cells by shortinterfering *** proliferation was evaluated by CCK-8 assay,and cell migration and invasion were detected by wound healing and Transwell *** expressions of proteins related to epithelial-mesenchymal transition were detected by western blot *** The expression of CASC20 was increased in GC tumor tissues and various GC cell *** CASC20 expression was correlated with a high risk of lymphatic metastasis and poor prognosis in GC *** vitro assays showed that silencing CASC20 reduced cell proliferation,migration,and invasion in GC *** studies revealed that CASC20 exhibits oncogenic functions by regulating MEMO1 expression through competitive endogenous binding to miR-143-5p,leading to induction of epithelial-mesenchymal *** Our findings indicate that CASC20 serves as a tumor promoter by regulating metastasis in GC via the miR-143-5p/MEMO1 ***20 may be a potential therapeutic target for GC.

关键词： Gastric cancer LncRNA Cancer susceptibility 20 miR-143-5p MEMO1 epithelialmesenchymal transition

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Salivary Fusobacterium nucleatum serves as a potential diagnostic biomarker for gastric cancer

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World Journal of Gastroenterology 2022年第30期28卷 4120-4132页

作者： Wen-Dan Chen Xin Zhang Meng-Jiao Zhang Ya-Ping Zhang Zi-Qi Shang Yi-Wei Xin Yi Zhang Department of Clinical Laboratory Qilu Hospital of Shandong UniversityJinan 250012Shandong ProvinceChina

BACKGROUND As one of the most common tumors,gastric cancer(GC)has a high mortality rate,since current examination approaches cannot achieve early *** nucleatum(Fn)primarily colonized in the oral cavity,has been reported to be involved in the development of gastrointestinal *** now,little is known about the relationship between salivary Fn and *** To determine whether salivary Fn could be a biomarker to diagnose GC and explore the influence of Fn on GC *** The abundance of Fn in saliva was quantified by droplet digital polymerase chain reaction in 120 GC patients,31 atrophic gastritis(AG)patients,35 non-AG(NAG)patients,26 gastric polyp(GP)patients,and 20 normal controls(NC)from Qilu Hospital of Shandong University from January 2019 to December *** operating characteristic(ROC)curve analysis was performed to evaluate the diagnostic value of Fn as well as traditional serum tumor markers,including carcinoembryonic antigen(CEA),carbohydrate antigen(CA)19-9,and *** assay and wound-healing assay were conducted to assess the influence of Fn infection on GC *** expression of epithelial-mesenchymal transition(EMT)markers was detected using western blot *** We found that the level of salivary Fn in GC patients was significantly increased compared with those in AG,NAG,and GP patients and NC(P<0.001).ROC curve analysis showed a favorable capability of Fn(73.33% sensitivity;82.14%specificity;area under the curve:0.813)in GC diagnosis,which was superior to that of CEA,CA19-9,CA72-4,ferritin,and sialic *** Fn level in saliva of GC patients was increased as the TNM stage *** patients with lymph node metastasis had higher Fn levels than those without *** transwell and wound-healing assays indicated that Fn infection promoted the migration and invasion of GC *** blot analysis showed that Fn infection decreased the expression of E-cadherin and increased the expressions of

关键词： Gastric cancer Fusobacterium nucleatum Saliva Prognosis Metastasis epithelialmesenchymal transition

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