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Metabolic landscape of human alveolar type II epithelial cells undergoing epithelial-mesenchymal transition induced directly by silica exposure

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Journal of Environmental Sciences 2025年第3期149卷 676-687页

作者： Jin Sun Na Zhao Ruijia Zhang Yizheng Li Tiantian Yu Qiying Nong Li Lin Xubin Yang Tiangang Luan Baowei Chen Yongshun Huang Southern Marine Science and Engineering Guangdong Laboratory School of Marine SciencesSun Yat-Sen UniversityZhuhai 519082China Guangdong Province Hospital for Occupational Disease Prevention and Treatment Guangzhou 510300China Guangdong Provincial Laboratory of Chemistry and Fine Chemical Engineering Jieyang Center Jieyang 515200China State Key Lab of Bioresource and Biocontrol School of Life ScienceSun Yat-sen UniversityGuangzhou 510275China Metabolic Innovation Center Zhongshan School of MedicineSun Yat-Sen UniversityGuangzhou 540080China Department of Endocrinology and Metabolism Guangdong Provincial Key Laboratory of DiabetologyThe Third Affiliated HospitalSun Yat-sen UniversityGuangzhou 510630China

epithelial-mesenchymal transition(EMT)plays an irreplaceable role in the development of ***,molecular mechanisms of EMT induced by silica exposure still remain to be ***,metabolic profiles of human alveolar type II epithelial cells(A549 cells)exposed directly to silica were characterized using non-targeted metabolomic approaches.A total of 84 differential metabolites(DMs)were identified in silica-treated A549 cells undergoing EMT,which were mainly enriched in metabolisms of amino acids(e.g.,glutamate,alanine,aspartate),purine metabolism,glycolysis,*** number of DMs identified in the A549 cells obviously increased with the elevated exposure concentration of ***,glutamine catabolism was significantly promoted in the silica-treated A549 cells,and the levels of related metabolites(e.g.,succinate)and enzymes(e.g.,α-ketoglutarate(α-KG)dehydrogenase)were substantially up-regulated,with a preference toα-KG *** of glutamine into the cell culture could substantially enhance the expression levels of both EMT-related markers and Snail(zinc finger transcription factor).Our results suggest that the EMT of human alveolar epithelial cells directly induced by silica can be essential to the development of silicosis.

关键词： Silica exposure Human alveolar type II epithelial cells(ATII cells) epithelial-mesenchymal transition (EMT) Metabolomics Glutamine

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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

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Transmembrane protein 176B promotes epithelial-mesenchymal transition in colorectal cancer through inflammasome inhibition

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World Journal of Gastrointestinal Oncology 2025年第3期17卷 171-187页

作者： Wei Qian Chong-Yi Xu Wei Hong Zhe-Ming Li Dao-Gun Xu Department of Proctology Wenling Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical UniversityWenling 317500Zhejiang ProvinceChina College of Life Sciences Zhejiang Chinese Medical UniversityHangzhou 310000Zhejiang ProvinceChina

BACKGROUND Activation of the epithelial-mesenchymal transition(EMT),a pivotal process in tumor metastasis and evasion,as well as the NLRP3 inflammasome,both promote colorectal cancer(CRC)*** studies have shown that Transmembrane protein 176B(TMEM176B)regulates NLRP3 and promotes CRC malignant *** To investigate the role of TMEM176B in modulating NLRP3 inflammasome and its implications on EMT and tumor progression in *** CRC in situ mouse and co-cultured cell models were established using CT26 cells,BALB/c mice,and primary cultured mouse natural killer(NK)*** hairpin RNA knocked down TMEM176B and NLRP3 expression in CT26 *** imaging,Terminal deoxynucleotidyl transferase dUTP nick end labeling assays,immunohistochemistry staining,flow cytometry,and molecular assays were used to investigate the effects of TMEM176B knockdown on the NLRP3 inflammasome in NK cells to assess tumor metastasis,apoptosis,and EMT *** Silencing TMEM176B in CRC mice significantly reduced tumor metastasis,proliferation,and EMT,while activating apoptosis,NLRP3 inflammasome,and NK cell ***,silencing TMEM176B in co-cultured cell models inhibited cell migration and invasion,and promoted *** interference of NLRP3 reversed these effects by modulating key proteins such as phosphorylated nuclear factor kappa B subunit 1 p65,matrix metallopeptidase 9,and transforming growth factor-β.CONCLUSION This study highlights the critical role of TMEM176B/NLRP3 in CRC progression and provides a basis for targeting this axis as a novel therapeutic approach to manage CRC progression and metastasis.

关键词： Transmembrane protein 176B epithelial-mesenchymal transition Colorectal cancer Pyrin domain containing 3 inflammasome Natural killer cell

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epithelial-mesenchymal transition-related circular RNAs in lung carcinoma

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Cancer Biology & Medicine 2021年第2期18卷 411-420页

作者： Meina Jiang Shuai Fang Xiaodong Zhao Chengwei Zhou Zhaohui Gong Department of Biochemistry and Molecular Biology Ningbo University School of MedicineNingbo 315211China Zhejiang Province Key Laboratory of Pathophysiology Ningbo University School of MedicineNingbo 315211China Department of Thoracic Surgery The Affiliated Hospital of Ningbo University School of MedicineNingbo 315020China

The epithelial-mesenchymal transition(EMT)is a highly complex phenotypic conversion during embryogenesis,and is important for metastasis,which contributes to tumor deterioration and poor prognoses of cancer *** carcinoma has a high tendency to develop the *** RNAs(circ RNAs)are involved in EMT-related cell invasion and metastasis in various types of ***,circ RNAs have been found to be a link to EMT-related transcription factors and EMT-associated signaling *** review mainly focuses on the influence of EMT-related circ RNAs on lung *** specifically,the roles of EMT-inducingand EMT-suppressive circ RNAs in lung carcinomas are *** circ RNAs potentially becoming promising biomarkers and therapeutic targets for cancer managements,they will hopefully stimulate the interest of medical workers in the early diagnosis,personalized treatment,and positive prognoses in the era of precision oncology.

关键词： epithelial-mesenchymal transition circular RNA transcription factor metastasis lung carcinoma

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SkullcapflavoneⅡsuppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro

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International Journal of Ophthalmology(English edition) 2025年第2期18卷 209-215页

作者： Meng-Xi Li Zhen Zhang Yue Zhang Fan-Ru Zhao Yu-Fan Li Yu-Fei Dang Yang-Yang Yue Li Li Department of Ophthalmology The First Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710061Shaanxi ProvinceChina Xi’an People’s Hospital(Xi’an Fourth Hospital) Shaanxi Eye HospitalAffiliated Xi’an Fourth HospitalNorthwestern Polytechnical UniversityXi’an 710000Shaanxi ProvinceChina Department of Vascular Surgery The First Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710061Shaanxi ProvinceChina

AIM:To investigate the effect of skullcapflavone II(SCF-II)on the epithelial-mesenchymal transition(EMT)induced by transforming growth factor beta(TGF-β)in human corneal epithelial cells(HCECs),as well as to identify the signaling pathways that may be ***:HCECs were cultured in *** a SCFII(5,10μmol/L)dose,cell viability was analysed with a cell counting kit-8(CCK-8)assay,and cell migration was monitored with wound healing and Transwell migration *** were 4 groups:SCF-II,TGF-β,SCF-II+TGF-βand *** blotting and immunofluorescence were performed to show the expression of EMT markers and the translocation of nuclear factor kappa-B(NF-κB)into the nucleus in the 4 ***:Treatment with SCF-II decreased HCEC viability in a dose-dependent manner.A concentration below 10μmol/L did not present obvious cell toxicity,and survival rates were more than 70%at *** with SCF-II(5 and 10μmol/L)significantly impeded migration in wound healing and Transwell migration assays(Pmesenchymal markers N-cadherin(P<0.05),α-smooth muscle actin(α-SMA;P<0.05)and NF-κB(P<0.05)in both TGF-β-and SCF-II-treated HCECs were lower than those in the HCECs treated with TGF-βalone and higher than those in HCECs treated with SCF-II *** showed that the entry of NF-κB into the nucleus in both TGF-β-and SCF-IItreated HCECs was less than that in the TGF-β-treated ***:SCF-II inhibit TGF-β-induced EMT in HCECs by potentially regulating the NF-κB signalling ***,SCF-II represents a candidate putative therapeutic agent in corneal fibrotic diseases.

关键词： skullcapflavone II epithelial-mesenchymal transition transforming growth factor nuclear factor kappa-B human corneal epithelial cells

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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

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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

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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

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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

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Transmembrane channel-like 5 drives hepatocellular carcinoma progression by regulating epithelial-mesenchymal transition

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World Journal of Clinical Oncology 2025年第3期16卷 68-82页

作者： Jiao Li Zi-Yu Wang Yan Jin Jing Xu Yun-Jin Ya Ting-Qiu Wan Xi Li Xi Wang Department of Hepatobiliary Surgery The Affiliated Hospital of Kunming University of Science and TechnologyKunming 650500Yunnan ProvinceChina

BACKGROUND Hepatocellular carcinoma(HCC)is a difficult cancer to manage due to its highly invasive and metastatic *** To investigate the molecular function of transmembrane channel-like 5(TMC5)in vitro and in vivo,with the objective of identifying novel diagnosis and treatment targets for *** The expression of TMC in cancer and normal tissues,along with its correlation with HCC prognosis,was analyzed using the GENT2,GEPIA database,and Human Protein *** analysis was conducted to assess the relationship between TMC5 expression and overall survival in TCGA-LIHC *** experiments were conducted to investigate the effect of TMC5 in cancer progression through loss-and gain-of-function assays in vitro and in *** Bioinformatics revealed that TMC5 expression was generally higher in tumors than in normal tissues,and its expression was associated with poorer patient survival ***5 expression in HCC tissues and cells was consistent with the results of the bioinformatics *** of TMC5 expression reduced migration,invasion,and proliferation,while also decreasing the expression of epithelial-mesenchymal transition(EMT)-associated molecules in MHCC97-LM3 ***,higher TMC5 expression significantly increased cell migration,invasion,proliferation,and EMT in MHCC97 L ***5 knockdown significantly decreased both the formation and spread of nodules in liver tissue,whereas TMC5 overexpression promoted *** Our study provides compelling evidence that TMC5 is highly expressed in HCC and drives cancer progression through the activation of EMT-mediated ***5 could represent a valuable molecular target for the diagnosis and treatment of HCC.

关键词： Hepatocellular carcinoma Transmembrane channel-like protein 5 epithelial-mesenchymal transition Bioinformatics diagnosis Prognosis

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