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Migfilin promotes migration and invasion in glioma by driving EGFR and MMP-2 signalings:A positive feedback loop regulation

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Journal of Genetics and Genomics 2017年第12期44卷 557-565页

作者： Yunwei Ou qingnan wu Chuanyue wu Xuefeng Liu Yongmei Song Qimin Zhan Department of Neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijing 100050China Beijing Neurosurgical Institute Capital Medical UniversityBeijing 100050China State Key Laboratory of Molecular Oncology National Cancer Center/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Department of Pathology University of PittsburghPittsburgh 15261USA Department of Biology and Shenzhen Key Laboratory of Cell Microenvironment South University of Science and Technology of ChinaShenzhen 518055China china National Clinical Research Center for Neurological Diseases BeUing 100050China

Glioma is the most common type of primary brain tumors in the central nervous system（CNS）. Migfilin occurs in human glioma and enhances cellular motility via the epidermal growth factor receptor（EGFR）pathway. However, the underlying molecular mechanism is not fully understood. In this study, we found that Migfilin promoted matrix metalloproteinase-2（MMP-2） activity, and restrained the expression of tissue inhibitor of metalloproteinase 2（TIMP2）, which is an MMP-2 inhibitor. Functional and structural studies showed that the LIM1 domain of Migfilin was required for Migfilin-mediated TIMP2 expression inhibition and MMP-2 activity, and was also necessary in promoting cell motility. Furthermore, Migfilininduced EGFR phosphorylation was greatly reduced by MMP-2 inhibitor（GM6001） or si RNA, while Migfilin-induced MMP-2 activation was also blocked by the EGFR inhibitor（AG1478） or si RNA. MMP-2 and EGFR inhibitors and their si RNAs can block Migfilin-induced migration and invasion, *** results demonstrated that EGFR and MMP-2 signalings may form a positive feedback loop to enhance Migfilin-induced migration and invasion. Finally, we detected that the expression of Migfilin,EGFR phosphorylation（Tyr1173） and MMP-2 activity had a positive correlation in the clinical glioma sample. Taken together, these results suggest that Migfilin is a critical regulator in cellular motility by driving the EGFR-MMP-2 feedback loop, and may be considered as a potential therapeutic target in glioma.

关键词： Glioma Migfilin MMP-2 EGFR Motility

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BAALC-AS1/G3BP2/c-Myc feedback loop promotes cell proliferation in esophageal squamous cell carcinoma

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Cancer Communications 2021年第3期41卷 240-257页

作者： Hongyue Zhang Yan Wang Weimin Zhang qingnan wu Jiawen Fan Qimin Zhan Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing 100142P.R.China Shenzhen Bay Laboratory ShenzhenGuangdong 518132P.R.China

Background:Long non-codingRNAs(lncRNAs)have been found to be involved in the development of many *** this study,we aimed to identify the molecular mechanisms of lncRNA BAALC antisense RNA 1(BAALC-AS1)in regulating the malignancy of esophageal squamous cell carcinoma(ESCC).Methods:The expression of BAALC-AS1 in cancer patients was analyzed using a tissue *** protein and RNA levels of BAALC-AS1 were determined by Western blotting analysis and quantitative reverse transcription-PCR(RT-qPCR),*** cell proliferation was determined by cell viability assays,bromodeoxyuridine incorporation,and flow *** relationships among BAALC-AS1,RasGAPSH3 domain-binding protein 2(G3BP2),and c-Myc were determined using RNA immunoprecipitation,RNA pull-down assays,and luciferase ***:The expression of BAALC-AS1 was highly up-regulated and associated with malignant phenotypes in ESCC tissues and cell *** vivo and in vitro assays showed that BAALC-AS1 promoted ESCC cell proliferation,migration,and ***-AS1 directly interacted with G3BP2,and thereby inhibited the degradation of c-Myc RNA 3’-UTR by G3BP2,thus leading to the accumulation of c-Myc ***,c-Myc acted as a transcription factor that can induce the expression of BAALC-AS1 by directly binding to its promoter ***:BAALC-AS1/G3BP2/c-Myc feedback loop plays a critical role in the development of ESCC,which might provide a novel therapeutic target and facilitate the development of new therapeutic strategies for the treatment of ESCC.

关键词： esophageal squamous cell carcinoma proliferation migration invasion long non-codingRNA BAALC-AS1 lncFZD6 G3BP2 c-Myc

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Src heterodimerically activates Lyn or Fyn to serve as targets for the diagnosis and treatment of esophageal squamous cell carcinoma

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Science China(Life Sciences) 2023年第6期66卷 1245-1263页

作者： Jing Zhang Di Zhao Lingyuan Zhang Yuanfan Xiao qingnan wu Yan Wang Jie Chen Qimin Zhan Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing100142China Peking University International Cancer Institute Peking UniversityBeijing100191China Research Unit of Molecular Cancer Research Chinese Academy of Medical SciencesBeijing100142China Institute of Cancer Research Shenzhen Bay LaboratoryShenzhen518107China

Although Src is one of the oldest and most investigated oncoproteins,its function in tumor malignancy remains to be defined *** this study,we demonstrated that the inhibition of Src activity by ponatinib effectively suppressed several malignant phenotypes of esophageal squamous cell carcinoma(ESCC)both in vitro and in vivo,whereas it did not produce growthinhibitory effects on normal esophageal epithelial cells(NEECs).Importantly,we combined phosphoproteomics and several cellular and molecular biologic strategies to identify that Src interacted with the members of Src-family kinases(SFKs),such as Fyn or Lyn,to form *** interactions with Fyn and Lyn phosphorylated the tyrosine sites in SH2(Fyn Tyr^(185)or Lyn Tyr^(183))and kinase domains(Fyn Tyr^(420) or Lyn Tyr^(397)),which critically contributed to ESCC *** contrast,Src could not form heterodimers with Fyn or Lyn in *** used RNA sequencing to comprehensively demonstrate that the inhibition of Src activity effectively blocked several critical tumor-promoting pathways,such as JAK/STAT,mTOR,stemness-related,and metabolism-related *** of the real-time polymerase chain reaction(RT-PCR)assay confirmed that Lyn and Fyn were critical effectors for the Src-mediated expression of tumor growth or metastasis-related ***,results of the clinical ESCC samples showed that the hyperactivation of pSrc Tyr^(419),Fyn Tyr^(185) or Tyr^(420),and Lyn Tyr^(183)or Tyr^(397)could be biomarkers of ESCC *** study illustrates that Src/Fyn and Src/Lyn heterodimers serve as targets for the treatment of ESCC.

关键词： esophageal squamous cell carcinoma heterodimer Src-family kinase Src tyrosine phosphorylation

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MAGE-C3 promotes cancer metastasis by inducing epithelial-mesenchymal transition and immunosuppression in esophageal squamous cell carcinoma

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Cancer Communications 2021年第12期41卷 1354-1372页

作者： qingnan wu Weimin Zhang Yan Wang Qingjie Min Hongyue Zhang Dezuo Dong Qimin Zhan Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing 100142P.R.China Shenzhen Bay Laboratory Institute of Cancer ResearchShenzhenGuangdong 518107P.R.China Research Unit of Molecular Cancer Research Chinese Academy of Medical SciencesBeijing 100142P.R.China Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Department of Radiation OncologyPeking University Cancer Hospital&InstituteBeijing 100142P.R.China

Background:Evading immune surveillance is necessary for tumor ***,there is an urgent need to better understand the interaction between metastasis and mechanisms of tumor immune *** this study,we aimed to clarify a novel mechanism that link tumor metastasis and immunosuppression in the development of esophageal squamous cell carcinoma(ESCC).Methods:The expression of melanoma-associated antigen C3(MAGE-C3)was detected using *** assays were used to evaluate the migration and invasion ability of esophageal squamous cell carcinoma(ESCC)*** assays in mice were used to evaluate metastatic ability in ***-mediated cytotoxicity assays were performed to visualize the immune suppression function on tumor *** sequencing was performed to identify differentially expressed genes between MAGE-C3 overexpressing ESCC cells and control *** ontology(GO)enrichment analyses was performed to identify the most altered pathways influenced by *** activation of the interferon-γ(IFN-γ)pathway was analyzed using Western blotting,GAS luciferase reporter assays,immunofluorescence,and flow *** role of MAGE-C3 in the IFN-γpathway was determined by Western blotting and ***,immunohistochemistry and flow cytometry analysis monitored the changes of infiltrated T cell populations in murine lung ***:MAGE-C3 was overexpressed in ESCC *** expression of MAGE-C3 had a significant association with the risk of lymphatic metastasis and poor survival in patients with *** experiments revealed that MAGE-C3 promoted tumor metastasis by activating the epithelial-mesenchymal transition(EMT).MAGE-C3 repressed antitumor immunity and regulated cytokine secretion of T cells,implying an immunosuppressive ***,MAGE-C3 facilitated IFN-γsignaling and upregulated programmed cell death ligand 1(PDŋL1)by binding with IFN-γreceptor 1(IFNGR1)and st

关键词： cancer metastasis epithelial-mesenchymal transition esophageal squamous cell carcinoma immunosuppression interferon-γreceptor interferon-γ melanoma-associated antigen C3

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Tumor-associated macrophage(TAM)-derived CCL22 induces FAK addiction in esophageal squamous cell carcinoma(ESCC)

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Cellular & Molecular Immunology 2022年第9期19卷 1054-1066页

作者： Jie Chen Di Zhao Lingyuan Zhang Jing Zhang Yuanfan Xiao qingnan wu Yan Wang Qimin Zhan Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing100142China Peking University International Cancer Institute Peking UniversityBeijing100191China Research Unit of Molecular Cancer Research Chinese Academy of Medical SciencesBeijingChina Institute of Cancer Research Shenzhen Bay LaboratoryShenzhen518107China

Tumor cell dependence on activated oncogenes is considered a therapeutic target,but protumorigenic microenvironment-mediated cellular addiction to specific oncogenic signaling molecules remains to be further ***,we showed that tumor-associated macrophages(TAMs)produced an abundance of C-C motif chemokine 22(CCL22),whose expression in the tumor stroma was positively associated with the level of intratumoral phospho-focal adhesion kinase(pFAK Tyr^(397)),tumor metastasis and reduced patient ***,CCL22-stimulated hyperactivation of FAK was correlated with increased malignant progression of cancer ***22-induced addiction to FAK was demonstrated by the persistent suppression of tumor progression upon FAK-specific ***,we identified that diacylglycerol kinaseα(DGKα)acted as a signaling adaptor to link the CCL22 receptor C-C motif chemokine receptor 4(CCR4)and FAK and promoted CCL22-induced activation of the FAK/AKT ***22/CCR4 signaling activated the intracellular Ca^(2+)/phospholipase C-γ1(PLC-γ1)axis to stimulate the phosphorylation of DGKαat a tyrosine residue(Tyr^(335))and promoted the translocation of DGKαto the plasma membrane to assemble the DGKα/FAK signalosome,which critically contributed to regulating sensitivity to FAK inhibitors in cancer *** identification of TAM-driven intratumoral FAK addiction provides opportunities for utilizing the tumor-promoting microenvironment to achieve striking anticancer effects.

关键词： Tumor-associated macrophages Esophageal squamous cell carcinoma FAK Oncogene addiction

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PAFR/Stat3 axis maintains the symbiotic ecosystem between tumor and stroma to facilitate tumor malignancy

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Acta Pharmaceutica Sinica B 2023年第2期13卷 694-708页

作者： Di Zhao Jing Zhang Lingyuan Zhang qingnan wu Yan Wang Weimin Zhang Yuanfan Xiao Jie Chen Qimin Zhan Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing 100142China Research Unit of Molecular Cancer Research Chinese Academy of Medical SciencesBeijing 100021China Peking University International Cancer Institute Beijing 100191China Shenzhen Bay Laboratory Shenzhen 518132China

Stroma surrounding the tumor cells plays crucial roles for tumor ***,little is known about the factors that maintain the symbiosis between stroma and tumor *** this study,we found that the transcriptional regulator-signal transducer and activator of transcription 3(Stat3)was frequently activated in cancer-associated fibroblasts(CAFs),which was a potent facilitator of tumor malignancy,and formed forward feedback loop with platelet-activating factor receptor(PAFR)both in CAFs and tumor ***,PAFR/Stat3 axis connected intercellular signaling crosstalk between CAFs and cancer cells and drove mutual transcriptional programming of these two types of *** central Stat3-related cytokine signaling molecules-interleukin 6(IL-6)and IL-11 played the critical role in the process of PAFR/Stat3 axis-mediated communication between tumor and *** inhibition of PAFR and Stat3 activities effectively reduced tumor progression using CAFs/tumor co-culture xenograft *** study reveals that PAFR/Stat3 axis enhances the interaction between tumor and its associated stroma and suggests that targeting this axis can be an effective therapeutic strategy against tumor malignancy.

关键词： Esophageal squamous cell carcinoma Cancer-associated fibroblasts PAFR Stat3 G-protein-coupled receptor JAK2 IL-6 IL-11

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Aqueous-soluble components of sporoderm-removed Ganoderma lucidum spore powder promote ferroptosis in oral squamous cell carcinoma

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Chinese Journal of Cancer Research 2023年第2期35卷 176-190页

作者： Xiangping wu qingnan wu Yan Wang Yehai Liu Zhenhao Li Qingchuan Liu Zhengming Huang Mingyan Li Bin Zhang Qimin Zhan Department of Otolaryngology-Head&Neck Surgery The First Affiliated Hospital of Anhui Medical UniversityHefei 230022China Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing 100142China Zhejiang Shouxiangu Pharmaceutical Co.Ltd Jinhua 321200China Beijing Weijian Jiye Institute of Biotechnology Beijing 102488China Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Head and Neck SurgeryPeking University Cancer Hospital&InstituteBeijing 100142China

Objective: Ferroptosis is a novel cell death process which displays a promising role in cancer ***, clinically available drugs targeting ferroptosis are rarely used, and yet there are no studies reporting on inducing ferroptosis via Chinese herbal extracts. Here we explored the tumor inhibition effects of Ganoderma lucidum(G. lucidum) on oral squamous cell carcinoma(OSCC). Specifically, we aimed to clarify the biological mechanism of components in the dietary, aqueous-soluble sporoderm-removed G. lucidum spore powder(A-GSP).Methods: Preliminary transcriptome analysis revealed the significant enrichment of the ferroptosis *** Fe2+, glutathione(GSH), malondialdehyde(MDA), reactive oxygen species(ROS) and lipid peroxide levels were measured to identify ferroptosis occurrence. Western blotting was used to measure ferroptosis-related proteins. Changes in mitochondria morphology and function were observed with transmission electron microscopy(TEM) and ATP detection assays. Ferroptosis inhibitor ferrostatin-1 was then used to verify the anti-tumor effects of A-GSP. Finally, nude mice xenograft models of oral cancer confirmed that A-GSP inhibited tumor ***: A-GSP promoted ferroptosis in oral cancer cells by inducing Fe2+influx, GSH depletion, as well as lipid peroxide and ROS accumulation. Ferroptosis-related proteins exhibited corresponding changes, particularly Acylco A synthetase long chain family member 4(ACSL4) increase and glutathione peroxidase 4(GPX4) decrease. A-GSP considerably lowered mitochondrial volume and ridge number, while significantly decreasing ATP production. Ferrostatin-1 reversed all of these A-GSP-induced changes. In vivo, A-GSP exerted a ferroptosismediated tumor-suppressing effect without observable adverse ***: Our findings demonstrate the therapeutic potential of A-GSP for treating patients with OSCC by targeting ferroptosis.

关键词： Ganoderma lucidum spore powder OSCC ferroptosis ACSL4

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Biphasic impacts of graphite-derived engineering carbon-based nanomaterials on plant performance:Effectiveness ***

Advanced Agrochem

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Advanced Agrochem 2023年第2期2卷 113-126页

作者： qingnan wu Chenjie Fan Hezhong Wang Yanlai Han Fuju Tai Jiakai wu Hui Li Rui He NanoAgro Center College of Plant ProtectionHenan Agricultural UniversityZhengzhou450002China College of Resources and Environmental Science Henan Agricultural UniversityZhengzhou450002China State Key Laboratory of Wheat and Maize Crop Science College of Life ScienceHenan Agricultural UniversityZhengzhou450002China

Graphite-derived carbon-based nanomaterials(GCNMs)as an exciting class of engineering carbonmaterials have been extensively exploited in environment and agriculture for pollution restorer,environmental purifier,plant growth stimulant,and stress resistance *** the increasing demand of production in past decades,GCNMs were inevitably released into the natural environment and became emerging *** review briefly summarized the recent progress on GCNMs-plant interaction with positive and negative sides,and discussed the biphasic(stimulatory-inhibitory)regulation of GCNMs on plant *** emphasis was placed on disseminating the latest scientific research,covering various effectiveness of GCNMs on plants and cells as well as ***,it is highlighted that fullerenes,carbon nanotubes,graphenes,and their functionalized forms as the representative zero-,one-,and two-dimensional GCNMs in optimum quantity have favorable efficacy on plants for seed germination,growth and development,fruit and productivity,and stress *** the contrary,GCNMs have possibly induced cytotoxicity and phytotoxicity on plant at anatomic,physiological,and genetic *** toxic mechanisms were mainly attributed to ion leakage from membrane,chloroplast damage,decreasing the levels of photosynthetic/nonphotosynthetic pigments and plant hormones,downregulating activities of metabolism and enzymatic/non-enzymatic antioxidant systems,or triggering ROS increase for inducing oxidative *** comprehensive review provides an in-depth insight of advanced progress made toward the utilization of GCNMs in plant science fields as well as current *** perspectives on a directional guide for further research in the emerging area of GCNMs-enabled phytonanotechnology are summarized at the *** will possibly provide an important reference role for further study and rational application of GCNMs in agriculture.

关键词： Carbon nanomaterial Graphite-derived Emerging pollutant Hormesis Phytotoxicity

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AKT2^(S128)/CCTα^(S315/319/323)-positive cancer-associated fibroblasts (CAFs) mediate focal adhesion kinase (FAK) inhibitors resistance via secreting phosphatidylcholines (PCs)

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Signal Transduction and Targeted Therapy 2024年第2期9卷 782-796页

作者： Jie Chen Lingyuan Zhang Yuheng Zhu Di Zhao Jing Zhang Yanmeng Zhu Jingyuan Pang Yuanfan Xiao qingnan wu Yan Wang Qimin Zhan Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&Institute100142 BeijingChina Peking University International Cancer Institute Peking University100191 BeijingChina Research Unit of Molecular Cancer Research Chinese Academy of Medical SciencesBeijingChina Soochow University Cancer Institute Suzhou 215000China Institute of Cancer Research Shenzhen Bay LaboratoryShenzhen 518107China

Abnormal metabolism is regarded as an oncogenic hallmark related to tumor progression and therapeutic *** study employed multi-omics,including phosphoproteomics,untargeted metabolomics and lipidomics,to demonstrate that the pAKT2 Ser128 and pCCTαSer315/319/323-positive cancer-associated fibroblasts(CAFs)substantially release phosphatidylcholines(PCs),contributing to the resistance of focal adhesion kinase(FAK)inhibitors in esophageal squamous cell carcinoma(ESCC)***,we observed extremely low levels of FAK Tyr397 expression in CAFs,potentially offering no available target for FAK inhibitors playing their anti-growth role in ***,FAK inhibitor increased the intracellular concentration of Ca2+in CAFs,promoting the formation of AKT2/CCTαcomplex,leading to phosphorylation of CCTαSer315/319/323 sites and eventually enhancing stromal PC *** activation could stimulate the intratumoral Janus kinase 2(JAK2)/Signal transducer and activator of transcription 3(STAT3)pathway,triggering resistance to FAK *** of clinical samples demonstrated that stromal pAKT2 Ser128 and pCCTαSer315/319/323 are related to the tumor malignancy and reduced patient ***-targeted lipidomics and further validation cohort quantitatively showed that plasma PCs enable to distinguish the malignant extent of ESCC *** conclusion,inhibition of stroma-derived PCs and related pathway could be possible therapeutic strategies for tumor therapy.

关键词： CAFs metabolism resistance

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CDK7-YAP-LDHD axis promotes D-lactate elimination and ferroptosis defense to support cancer stem cell-like properties

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Signal Transduction and Targeted Therapy 2023年第9期8卷 4346-4364页

作者： Mengzhu Lv Ying Gong Xuesong Liu Yan Wang qingnan wu Jie Chen Qingjie Min Dongyu Zhao Xianfeng Li Dongshao Chen Di Yang Danna Yeerken Rui Liu Jinting Li Weimin Zhang Qimin Zhan Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education) Department of Molecular OncologyPeking University Cancer Hospital and InstituteBeijing 100142China Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education) Department of Breast OncologyPeking University Cancer Hospital and InstituteBeijing 100142China Research Unit of Molecular Cancer Research Chinese Academy of Medical SciencesBeijing 100021China Peking University International Cancer Institute Beijing 100191China Institute of Cancer Research Shenzhen Bay LaboratoryShenzhen 518107China Department of Oncology Cancer InstitutePeking University Shenzhen HospitalShenzhen Peking University-Hong Kong University of Science and Technology(PKU-HKUST)Medical CenterShenzhen 518036China Soochow University Cancer Institute Suzhou 215127China

Reprogrammed cellular metabolism is essential for maintaining cancer stem cells(CSCs)***,we report that mitochondrial D-lactate catabolism is a necessary initiating oncogenic event during tumorigenesis of esophageal squamous cell carcinoma(ESCC).We discover that cyclin-dependent kinase 7(CDK7)phosphorylates nuclear Yes-associated protein 1(YAP)at S127 and S397 sites and enhances its transcription function,which promotes D-lactate dehydrogenase(LDHD)protein ***,LDHD is enriched significantly in ESCC-CSCs rather than differentiated tumor cells and high LDHD status is connected with poor prognosis in ESCC ***,the CDK7-YAP-LDHD axis helps ESCC-CSCs escape from ferroptosis induced by D-lactate and generates pyruvate to satisfy energetic demands for their elevated self-renewal ***,we conclude that esophageal CSCs adopt a D-lactate elimination and pyruvate accumulation mode dependent on CDK7-YAP-LDHD axis,which drives stemness-associated hallmarks of ***,targeting metabolic checkpoints may serve as an effective strategy for ESCC therapy.

关键词： esophageal metabolism elevated

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