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epithelial-mesenchymal transition mediated tumourigenesis in the gastrointestinal tract

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World Journal of Gastroenterology 2008年第24期14卷 3792-3797页

作者： Ammar Natalwala Robert Spychal Chris Tselepis The Medical School University of Birmingham Sandwell and West Birmingham Hopsitals NHS Trust CRUK Institute for Cancer Studies University of Birmingham

epithelial-mesenchymal transition (EMT) is a highly conserved process that has been well characterised in embryogenesis. Studies have shown that the aberrant activation of EMT in adult epithelia can promote tumour metastasis by repressing cell adhesion molecules,including epithelial (E)-cadherin. Reduced intracellular adhesion may allow tumour cells to disseminate and spread throughout the body. A number of transcription proteins of the Snail superfamily have been implicated in EMT. These proteins have been shown to be over-expressed in advanced gastrointestinal (GI) tumours including oesophageal adenocarcinomas,colorectal carcinomas,gastric and pancreatic cancers,with a concomitant reduction in the expression of E-cadherin. Regulators of EMT may provide novel clinical targets to detect GI cancers early,so that cancers previously associated with a poor prognosis such as pancreatic cancer can be diagnosed before they become inoperable. Furthermore,pharmacological therapies designed to inhibit these proteins will aim to prevent local and distant tumour invasion.

关键词： epithelial-mesenchymal transition Transcription proteins E-cadherin Gastrointestinalcancer

epithelial-mesenchymal transition contributes to malignant phenotypes of circulating tumor cells derived from gastric cancer

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BIOCELL 2019年第4期43卷 293-298页

作者： TIANGEN WU TIANHAO BAO DAOMING LIANG LIN WANG Department of Gastrointestinal Surgery the Second Affiliated Hospital of Kunming Medical UniversityKunming650101China Biomedical Engineering University of AlbertaEdmontonAlbertaCanada Mental Health Center of Kunming Medical University Kunming650224China Department of Hepatobiliary Surgery the Second Affiliated Hospital of Kunming Medical UniversityKunming650101China

Circulating tumor cells(CTCs)are crucial to tumor metastasis,and they usually undergo epithelial-mesenchymal transition(EMT)in order to disseminate from the primary ***,very little is currently known about the relationship between EMT and malignant phenotypes of CTCs in the context of gastric ***,this study aimed to investigate the contribution of EMT to malignant phenotypes of CTCs derived from gastric cancer *** xenografted MKN28 gastric cancer cells pretreated with transforming growth factor-beta 1(TGFβ-1)into nude mice by intravenous ***,we isolated CTCs from the blood of nude mice by gradient centrifugation and found that CTCs derived from MKN28 cells pretreated with TGFβ-1 had a significantly increased viability and invasion ability compared to MKN28 cells without TGFβ-1 *** staining showed lower expression of E-cadherin and higher expression of N-cadherin,vimentin,and β-catenin in CTCs derived from MKN28 cells pretreated with TGFβ-***,the expression of Wnt3a,β-catenin,cyclin D1,and c-Myc was significantly higher in CTCs derived from MKN28 cells pretreated with TGFβ-*** together,these findings suggest that TGFβ promotes EMT and malignant phenotypes of gastric cancer ***,the malignant phenotypes of gastric cancer cells induced by TGFβ are maintained in CTCs derived from these *** EMT in CTCs is a new approach to the treatment of gastric cancer relapse and metastasis.

关键词： Circulating tumor cells epithelial-mesenchymal transition Gastric cancer

epithelial-mesenchymal transition as a therapeutic target for overcoming chemoresistance in pancreatic cancer

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World Journal of Gastrointestinal Oncology 2017年第1期9卷 37-41页

作者： Omar Elaskalani Norbaini Binti Abdol Razak Marco Falasca Pat Metharom Platelet Research Laboratory Curtin Health Innovation and Research Institute Department of Health Sciences Curtin University School of Biomedical Sciences Curtin Health Innovation Research Institute Curtin University Metabolic Signalling Group School of Biomedical Sciences Curtin Health Innovation Research InstituteCurtin University

Pancreatic cancer has one of the worst prognoses among all cancers due to the late manifestation of identifiable symptoms and high resistance to chemo- and radiation therapies. In recent years, a cancer development phase termed epithelial-mesenchymal transition(EMT) has gained increasing research focus. The process is implicated in tumour metastasis, and emerging evidence suggests EMT also contributes or induces chemoresistance in several cancers. Nevertheless, the applicability of therapeutic targeting of EMT faces many challenges. In this mini-review, we summarise the evidence supporting the role of EMT in pancreatic cancer progression, focusing particularly on its association with chemoresistance.

关键词： epithelial-mesenchymal transition Drug resistance Pancreatic cancer Chemotherapy

epithelial-mesenchymal transition:a hallmark in pancreatic cancer stem cell migration,metastasis formation,and drug resistance

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Journal of Cancer Metastasis and Treatment 2020年第1期6卷 425-439页

作者： Ahmad R.Safa Department of Pharmacology and Toxicology Indiana University School of MedicineIndianapolisIN46202USA

Metastasis,tumor progression,and chemoresistance are the major causes of death in patients with pancreatic ductal adenocarcinoma(PDAC).Tumor dissemination is associated with the activation of an epithelial-tomesenchymal transition(EMT)process,a program by which epithelial cells lose their cell polarity and cell-tocell adhesion,and acquire migratory and invasive abilities to become mesenchymal stem cells(MSC).These MSCs are multipotent stromal cells capable of differentiating into various cell types and trigger the phenotypic transition from an epithelial to a mesenchymal ***,EMT promotes migration and survival during cancer metastasis and confers stemness features to particular subsets of ***,a major problem limiting our ability to treat PDAC is the existence of rare populations of pancreatic cancer stem cells(PCSCs)or cancer-initiating cells in pancreatic *** may represent sub-populations of tumor cells resistant to therapy which are most crucial for driving invasive tumor *** cells are capable of regenerating the cellular heterogeneity associated with the primary tumor when xenografted into ***,the presence of PCSCs has prognostic relevance and influences the therapeutic response of *** express markers of cancer stem cells(CSCs)including CD24,CD133,CD44,and epithelial specific antigen as well as the drug transporter ABCG2 grow as spheroids in a defined growth medium.A major difficulty in studying tumor cell dissemination and metastasis has been the identification of markers that distinguish metastatic cancer cells from cells that are normally circulating in the bloodstream or at sites where these cells *** highlights a linkage between CSC and *** this review,The current understanding of the PCSCs,signaling pathways regulating these cells,PDAC heterogeneity,EMT mechanism,and links between EMT and metastasis in PCSCs are *** information may provide potential therapeutic s

关键词： Pancreatic cancer cancer stem cells epithelial-mesenchymal transition metastasis drug resistance

RGS4 promotes the progression of gastric cancer through the focal adhesion kinase/phosphatidyl-inositol-3-kinase/protein kinase B pathway and epithelial-mesenchymal transition

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World Journal of Gastroenterology 2025年第2期31卷 113-127页

作者： Peng-Yu Chen Pei-Yao Wang Bang Liu Yang-Pu Jia Zhao-Xiong Zhang Xin Liu Dao-Han Wang Yong-Jia Yan Wei-Hua Fu Feng Zhu Department of General Surgery Tianjin Medical University General HospitalTianjin Medical UniversityTianjin 300052China Department of General Surgery Jincheng People’s HospitalJincheng 048000Shanxi ProvinceChina

BACKGROUND Regulator of G protein signaling(RGS)proteins participate in tumor formation and metastasis by acting on theα-subunit of heterotrimeric G *** speci-fic effect of RGS,particularly RGS4,on the progression of gastric cancer(GC)is not yet *** To explore the role and underlying mechanisms of action of RGS4 in GC *** The prognostic significance of RGS4 in GC was analyzed using bioinformatics based public databases and verified by immunohistochemistry and quantitative polymerase chain reaction in 90 patients with *** assays were employed to assess the carcinogenic impact of RGS4,and the mechanism of its possible influence was detected by western blot analysis.A nude mouse xenograft model was established to study the effects of RGS4 on GC growth in *** RGS4 was highly expressed in GC tissues compared with matched adjacent normal *** RGS4 expression was correlated with increased tumor-node-metastasis stage,increased tumor grade as well as poorer overall survival in patients with *** experiments demonstrated that RGS4 knockdown suppressed GC cell proliferation,migration and ***,xenograft experiments confirmed that RGS4 silencing significantly inhibited tumor ***,RGS4 knockdown resulted in reduced phosphorylation levels of focal adhesion kinase,phosphatidyl-inositol-3-kinase,and protein kinase B,decreased vimentin and N-cadherin,and elevated *** High RGS4 expression in GC indicates a worse prognosis and RGS4 is a prognostic ***4 influences tumor progression via the focal adhesion kinase/phosphatidyl-inositol-3-kinase/protein kinase B pathway and epithelial-mesenchymal transition.

关键词： Gastric cancer Prognosis Regulator of G protein signaling 4 Focal adhesion kinase epithelial-mesenchymal transition

Palladium nanoplates scotch breast cancer lung metastasis by constraining epithelial-mesenchymal transition

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National Science Review 2021年第7期8卷 124-136页

作者： Shunhao Wang Jingchao Li Mei Chen Liting Ren Wenya Feng Lining Xu Xiaolan Chen Tian Xia Nanfeng Zheng Sijin Liu State Key Laboratory of Environmental Chemistry and Ecotoxicology Research Center for Eco-Environmental Sciences Chinese Academy of Sciences University of Chinese Academy of Sciences State Key Laboratory for Physical Chemistry of Solid Surfaces Collaborative Innovation Center of Chemistry for Energy Materials Department of Chemistry Xiamen University College of Materials Science and Engineering Hunan University Division of Nanomedicine Department of Medicine California Nano Systems Institute University of CaliforniaLos Angeles

Metastasis accounts for the majority of cancer deaths in many tumor types including breast ***-mesenchymal transition(EMT) is the driving force for the occurrence and progression of metastasis, however, no targeted strategies to block the EMT program are currently available to combat metastasis. Diverse engineered nanomaterials(ENMs) have been reported to exert promising anti-cancer effects, however, no ENMs have been designed to target EMT. Palladium(Pd) nanomaterials, a type of ENM, have received substantial attention in nanomedicine due to their favorable photothermal performance for cancer therapeutics. Herein, Pd nanoplates(Pd PL) were found to be preferentially biodistributed to both primary tumors and metastatic tumors. Importantly, Pd PL showed a significant inhibition of lung metastasis with and without near-infrared(NIR) irradiation. Mechanistic investigations revealed that EMT was significantly compromised in breast cancer cells upon the Pd PL treatment, which was partially due to the inhibition of the transforming growth factor-beta(TGF-β) signaling. Strikingly, the Pd PL was found to directly interact with TGF-β proteins to diminish TGF-β functions in activating its downstream signaling, as evidenced by the reduced phosphorylation of Smad2. Notably,TGF-β-independent pathways were also involved in undermining EMT and other important biological processes that are necessary for metastasis. Additionally, NIR irradiation elicited synergistic effects on PdPL-induced inhibition of primary tumors and metastasis. In summary, these results revealed that the Pd PL remarkably curbed metastasis by inhibiting EMT signaling, thereby indicating the promising potential of Pd PL as a therapeutic agent for treating breast cancer metastasis.

关键词： palladium nanoplates tumor targeting lung metastasis epithelial-mesenchymal transition TGF-β

Perfluorooctane sulfonate promotes the migration of colorectal cancer cells by inducing epithelial-mesenchymal transition

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Journal of Environmental Sciences 2024年第11期145卷 1-12页

作者： Fangfang Li Lu Chen Bi-Xia Peng Yuyang Lei Minjie Li Liang-Hong Guo Institute of Environmental and Health Sciences China Jiliang UniversityHangzhou 310018China Key Laboratory of Pollution Exposure and Health Intervention of Zhejiang Province Hangzhou 310015China College of Quality and Safety Engineering China Jiliang UniversityHangzhou 310018China College of Life Sciences China Jiliang UniversityHangzhou 310018China

The potential association between colorectal cancer(CRC)and environmental pollutants is *** studies have found that some perfluoroalkyl acids,including perfluorooctane sulfonate(PFOS),induced colorectal tumors in experimental animals and promoted the migration of and invasion by CRC cells in vitro,but the underlying mechanism is ***,we investigated the effects of PFOS on the proliferation and migration of CRC cells and the potentialmechanisms involving activating the PI3K/Akt-NF-κB signal pathway and epithelial-mesenchymal transition(EMT).It was found that PFOS promoted the growth andmigration of HCT116 cells at non-cytotoxic concentrations and increased the mRNA expression of the migration-related angiogenic cytokines vascular endothelial growth factor(VEGF)and interleukin-8(IL-8).In a mechanistic investigation,the up-stream signal pathway PI3K/Akt-NF-κB was activated by PFOS,and the process was suppressed by LY294002(PI3K/Akt inhibitor)and BAY11-7082(NF-κB inhibitor)respectively,leading to less proliferation of HCT116 ***,matrix metalloproteinases(MMP)and EMT-related markers were up-regulated after PFOS exposure,and were also suppressed respectively by LY294002 and ***,the up-regulation of EMT markers was suppressed by a MMP inhibitor *** together,our results indicated that PFOS promotes colorectal cancer cell migration and proliferation by activating the PI3K/Akt-NF-κB signal pathway and epithelial-mesenchymal *** could be a potential toxicological mechanism of PFOS-induced malignant development of colorectal cancer.

关键词： Perfluorooctane sulfonate Colorectal cancer Cell migration PI3K/Akt-NF-κB epithelial-mesenchymal transition

Loss of lncRNA SNHG8 promotes epithelial-mesenchymal transition by destabilizing CDH1 mRNA

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Science China(Life Sciences) 2021年第11期64卷 1858-1867页

作者： Ping He Cheng Zhang Guoqiang Chen Shaoming Shen Department of Pathophysiology Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of EducationState Key Laboratory of Oncogenes and Related Genes and Chinese Academy of Medical Sciences Research Unit(NO.2019RU043)Shanghai Cancer InstituteRui-Jin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China

Long non-coding RNAs(lnc RNAs) are widely involved in a variety of biological processes, including epithelial-mesenchymal transition(EMT). In the current study, we found that lnc RNA small nucleolar RNA host gene 8(SNHG8) was tightly correlated with EMT-associated gene signatures, and was down-regulated by Zinc finger E-box-binding homeobox 1(ZEB1) during EMT progress. Functionally, knockdown of SNHG8 induced EMT in epithelial cells, through destabilizing the CDH1 m RNA dependent on a 17-nucleotide sequence shared by SNHG8 and CDH1. In addition, analysis with public database showed that SNHG8 tended to be down-regulated in different cancer types and the lower expression of SNHG8 predicted poorer *** together, our study reports a ZEB1-repressed lnc RNA SNHG8 which is important for stabilizing CDH1 m RNA, thereby maintaining the epithelial status of epithelial cells.

关键词： SNHG8 epithelial-mesenchymal transition CDH1 mRNA stability

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*** mycelium inhibits epithelial–mesenchymal transition by inactivating the midkine pathway in pulmonary fibrosis

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Frontiers of Medicine 2021年第2期15卷 313-329页

作者： Li Lu Haiyan Zhu Hailin Wang Huaping Liang Yayi Hou Huan Dou The State Key Laboratory of Pharmaceutical Biotechnology Division of ImmunologyMedical SchoolNanjing UniversityNanjing 210093China Department of Rheumatology and Immunology Nanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical SchoolNanjing 210008China State Key Laboratory of Trauma Burns and Combined InjuryResearch Institute of SurgeryDaping HospitalThe Army Medical UniversityChongqing 400042China Jiangsu Key Laboratory of Molecular Medicine Nanjing UniversityNanjing 210093China

The medical fungus Hirsutella sinensis has been used as a Chinese folk health supplement because of its immunomodulatory *** previous studies established the antifibrotic action of Hirsutella sinensis mycelium(HSM)in the *** epithelial–mesenchymal transition(EMT)is involved in the pathogenesis of idiopathic pulmonary *** present study investigates the role of HSM in mediating EMT during the development of pulmonary *** significantly inhibits bleomycin(BLM)-induced pulmonary fibrosis by blocking the *** addition,the expression levels of midkine are increased in the lungs of the BLM-induced *** analysis of the results indicates that the mRNA level of midkine correlated positively with *** markedly abrogates the transforming growth factorβ-induced EMT-like phenotype and behavior in *** activation of midkine related signaling pathway is ameliorated following HSM treatment,whereas this extract also caused an effective attenuation of the induction of EMT(caused by midkine overexpression)in *** further confirm that oral medication of HSM disrupted the midkine pathway in ***,findings suggest that the midkine pathway and the regulation of the EMT may be considered novel candidate therapeutic targets for the antifibrotic effects caused by HSM.

关键词： epithelial-mesenchymal transition H.sinensis mycelium midkine pulmonary fibrosis

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