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| 1 | Snail and Slug mediate tamoxifen resistance in breast cancer cells through activation of EGFR-ERK independent of epithelial-mesenchymal transition显示文摘 | Yan Jian Xiaotong Zhao Qian Xiao Qingbo Liu Keshuo Ding Fei Yu Rui Zhang Tao Zhu Gaoxiang Ge | 2014 | Journal of Molecular Cell Biology2014，8，4： | 11 |
| 2 | LKB1 in lung cancerigenesis:a serine/threonine kinase as tumor suppressor显示文摘Lung cancer is featured with high mortality,with a 15%five-year survival rate worldwide.Genetic alterations,such as loss of function of tumor suppressor genes,frequently contribute to lung cancer initiation,progression and metastasis.Liver kinase B1(LKB1),as a serine/threonine kinase and tumor suppressor,is frequently mutated and inactivated in non-small cell lung cancer(NSCLC).Recent studies have provided strong evidences that LKB1 loss promotes lung cancerigenesis process,especially lung cancer progression and metastasis.This review will summarize recent progress on how LKB1 modulates the process of lung cancerigenesis,emphasizing on LKB1 downstream signaling pathways and biological functions.We will further discuss the potential development of prognostic biomarkers or therapeutic targets in lung cancer clinic based on the molecular alteration associated with deregulated LKB1 signaling. | Yijun Gao Gaoxiang Ge Hongbin Ji | 2011 | Protein & Cell2011，2，2： | 8 |
| 3 | Lysyl oxidase promotes bleomycin-induced lung fibrosis through modulating inflammation显示文摘包括 lysyl oxidase (哈鱼) ,涉及骨胶原生合成的酶为自发的肺的纤维变性作为潜在的治疗学的目标被建议了。哈鱼表示是显著地,在 bleomycin (BLM ) 的 upregulated 导致了肺纤维变性,并且哈鱼表示或哈鱼活动的抑制击倒减轻肺纤维变性。出人意料地,有在煽动性的阶段的哈鱼禁止者的鼠标的治疗,然而并非 fibrogenic 阶段,高效地减少骨胶原免职并且使肺建筑学正常化。哈鱼的抑制损害煽动性的房间渗入,发信号的 TGF- ,和 myofibroblast 累积。而且,哈鱼的宫外的表示敏化纤维变性抵抗的 Balb/c 老鼠到导致 BLM 的发炎和肺纤维变性。这些结果建议那条哈鱼为由在肺损害以后加重煽动性的反应和随后的纤维变性过程的导致 BLM 的试验性的肺纤维变性的前进是不可缺少的。 | Tao Cheng Qingbo Liu Rui Zhang Ying Zhang Jianfeng Chen Ronghuan Yu Gaoxiang Ge | 2014 | Journal of Molecular Cell Biology2014，8，6： | 3 |
| 4 | IntegrinαEβ7^(+)T cells direct intestinal stem cell fate decisions via adhesion signaling显示文摘Intestinal stem cell(ISC)differentiation is regulated precisely by a niche in the crypt,where lymphocytes may interact with stem and transient amplifying(TA)cells.However,whether and how lymphocyte–stem/TA cell contact affects ISC differentiation is largely unknown.Here,we uncover a novel role of T cell–stem/TA cell contact in ISC fate decisions.We show that intestinal lymphocyte depletion results in skewed ISC differentiation in mice,which can be rescued by T cell transfer.Mechanistically,integrinαEβ7 expressed on T cells binds to E-cadherin on ISCs and TA cells,triggering E-cadherin endocytosis and the consequent Wnt and Notch signaling alterations.BlockingαEβ7−E-cadherin adhesion suppresses Wnt signaling and promotes Notch signaling in ISCs and TA cells,leading to defective ISC differentiation.Thus,αEβ7^(+)T cells regulate ISC differentiation at single-cell level through cell–cell contact-mediatedαEβ7−E-cadherin adhesion signaling,highlighting a critical role of the T cell–stem/TA cell contact in maintaining intestinal homeostasis. | Shiyang Chen Yajuan Zheng Xiaojuan Ran Hui Du Hua Feng Lei Yang Yating Wen Changdong Lin Shihui Wang Mengwen Huang Zhanjun Yan Dianqing Wu Hongyan Wang Gaoxiang Ge An Zeng Yi Arial Zeng Jianfeng Chen | 2021 | Cell Research2021，31，12： | 3 |
| 5 | Protein C receptor is a therapeutic stem cell target in a distinct group of breast cancers显示文摘Breast cancer is a heterogeneous disease.In particular,triple-negative breast cancer(TNBC)comprises various molecular subgroups with unclear identities and currently has few targeted treatment options.Our previous study identified protein C receptor(Procr)as a surface marker on mammary stem cells(MaSCs)located in the basal layer of the normal mammary gland.Given the possible connection of TNBC with basal layer stem cells,we conducted comparative analyses of Procr in breast cancers of mouse and human origin.In mouse mammary tumors,we showed that Procr+cells are enriched for cancer stem cells(CSCs)in Wnt1 basal-like tumors,but not in Brea basal-like tumors or PyVT luminal tumors.In human cancers,PROCR was robustly expressed in half of TNBC cases.Experiments with patient-derived xenografts(PDXs)revealed that PROCR marks CSCs in this discrete subgroup(referred to as PROCR+TNBC).Interfering with the function of PROCR using an inhibitory nanobody reduced the CSC numbers,arrested tumor growth and prevented rapid tumor recurrence.Our data suggest a key role of MaSC in breast tumorigenesis.Moreover,our work indicates that PROCR can be used as a biomarker to stratify TNBC into clinically relevant subgroups and may provide a novel targeted treatment strategy for this clinically important tumor subtype. | Daisong Wang Xin Hu Chunye Liu Yingying Jia Yiqin Bai Cheguo Cai Jingqiang Wang Lanyue Bai Ruikai Yang ChangDong Lin Yi-Rong Liu Shan Li Feng Qiao Ling Yao Li Chen Gaoxiang Ge Hai Jiang Dianfan Li Lin Li JianFeng Chen Zhi-Ming Shao Yi Arial Zeng | 2019 | Cell Research2019，29，10： | 2 |
| 6 | Lysyl Oxidase, ingand Cancer Metastasis显示文摘 | Qian Xiao Gaoxiang Ge | 2012 | Cancer Mi Extraeellular Matrix Remodel- t2012，5，： | 1 |
| 7 | Lymphocyte integrins mediate entry and dysregulation of T cells by SARS-CoV-2显示文摘Dear Editor,T-cell infection by SARS-CoV-2 and associated immune responses are correlated with disease severity and prognosis of COVID-19.Lymphopenia is associated with increased disease severity in COVID-19.Significantly lower circulating T and B cell counts were observed in patients who died from COVID-19 compared with survivors.Moreover,SARS-CoV-2 infection causes aberrant lymphocyte activation and dysfunction. | Mengwen Huang Xingchao Pan Xinling Wang Qingfei Ren Bei Tong Xianchi Dong Gaoxiang Ge Lu Lu Shibo Jiang Jianfeng Chen | 2023 | Signal Transduction and Targeted Therapy2023，8，3： | 0 |
| 8 | 发热通过Hsp90-α4整合素热感应信号通路促进T淋巴细胞迁移显示文摘文章简介发热是机体受到病原体感染、产生损伤或者炎症后的一种复杂的生理应激反应。发热可以促进淋巴细胞迁移到次级淋巴器官或者炎症部位而促进免疫反应,对免疫稳态维持和免疫监视非常重要,但是目前对发热调控淋巴细胞黏附和迁移的机制还不清楚。本研究中,课题组发现:发热可以通过热休克蛋白90(heat shock protein 90,Hsp90)诱导α4整合素活化并传递下游信号通路。 | 林昶东 张有华 Kun Zhang YaJuan Zheng Ling Lu HaiShuang Chang Hui Yang YanRong Yang YaoYing Wan ShiHui Wang MengYa Yuan ZhanJun Yan RongGuang Zhang YongNing He GaoXiang Ge Dianqing Wu 陈剑峰 | 2020 | 科学新闻2020，，2： | 0 |
| 9 | Exploring the underlying biology of cancer and potential therapeutic strategies:a special issue focused on mechanism-based studies显示文摘Cancer,commonly referred to as malignant tumors,is one of the deadliest human diseases.Every year,millions of people die from cancer,and almost as many are newly diagnosed with the disease.Due to its severe impact on both individuals and the economy,cancer research has become one of the most active areas of biomedical research in recent decades.As cancer originates from highly proliferative,invasive,and immune-suppressive transformed cells,understanding the molecular mechanisms that determine the malignant phenotype of cancer cells is crucial for the development of effective cancer therapy.This special issue comprises 10 reviews by experts in basic cancer research and aims at summarizing the up-todate advances in cancer biology from their own perspectives. | Daming Gao Gaoxiang Ge | 2023 | Acta Biochimica et Biophysica Sinica2023，55，6： | 0 |
| 10 | Intact regulation of G1/S transition renders esophageal squamous cell carcinoma sensitive to PI3Kαinhibitors显示文摘Phosphatidylinositol 3-kinase alpha(PI3Kα)inhibitors are currently evaluated for the therapy of esophageal squamous cell carcinoma(ESCC).It is of great importance to identify potential biomarkers to predict or monitor the efficacy of PI3Kαinhibitors in an aim to improve the clinical responsive rate in ESCC.Here,ESCC PDXs with CCND1 amplification were found to be more sensitive to CYH33,a novel PI3Kα-selective inhibitor currently in clinical trials for the treatment of advanced solid tumors including ESCC.Elevated level of cyclin D1,p21 and Rb was found in CYH33-sensitive ESCC cells compared to those in resistant cells.CYH33 significantly arrested sensitive cells but not resistant cells at G1 phase,which was associated with accumulation of p21 and suppression of Rb phosphorylation by CDK4/6 and CDK2.Hypo-phosphorylation of Rb attenuated the transcriptional activation of SKP2 by E2F1,which in turn hindered SKP2-mediated degradation of p21 and reinforced accumulation of p21.Moreover,CDK4/6 inhibitors sensitized resistant ESCC cells and PDXs to CYH33.These findings provided mechanistic rationale to evaluate PI3Kαinhibitors in ESCC patients harboring amplified CCND1 and the combined regimen with CDK4/6 inhibitors in ESCC with proficient Rb. | Xu Zhang Yuxiang Wang Xi Zhang Yanyan Shen Kang Yang Qingyang Ma Yuemei Qiao Jiajie Shi Yi Wang Lan Xu Biyu Yang Gaoxiang Ge Landian Hu Xiangyin Kong Chunhao Yang Yi Chen Jian Ding Linghua Meng | 2023 | Signal Transduction and Targeted Therapy2023，8，5： | 0 |
| 11 | Non-radioisotopic method for the in vitro measurement of EGF receptor tyrosine kinase显示文摘A non-radioisotopic method was developed for the assay of epidermal growth factor receptor (EGFR). A peptide with twenty amino acid residues around Tyr 1173, the major phosphorylation site of EGFR, was cloned as a GST fusion protein and used as substrate. Anti-phosphoty-rosine monoclonal antibody PY99 was used for the determination of the extent of phosphorylation. Both the specificity and the sensitivity were substantially higher than that of the existing method. Km value of the fusion protein is much lower (10 μmol/L) than that of the synthetic peptide (110 μmol/L). The method can be applied to the measurement of the tyrosine kinase activity of c-erb B2 (Neu/HER2). | Gaoxiang Ge Jing Wu Qishui Lin | 2001 | Chinese Science Bulletin2001，46，8： | 0 |
| 12 | Basement membrane promotes tumor development by attenuating T cell activation显示文摘Dear Editor,T cells recognize and eliminate cancer cells.Prolonged survival of cancer patients is associated with not only intratumoral T cell infiltration but also the functional status of infiltrated T cells(Galon and Bruni,2020).The immune contexture,including the number and functionality of T cells,is modulated by the tumor microenvironment(Joyce and Fearon,2015;Galon and Bruni,2020). | Xiangming Liu Yuemei Qiao JianFeng Chen Gaoxiang Ge | 2022 | Journal of Molecular Cell Biology2022，14，2： | 0 |
| 13 | Type IV collagen α5 chain promotes luminal breast cancer progression through c-Myc-driven glycolysis显示文摘Cancer cell metabolism reprogramming is one of the hallmarks of cancer.Cancer cells preferentially utilize aerobic glycolysis,which is regulated by activated oncogenes and the tumor microenvironment.Extracellular matrix(ECM)in the tumor microenvironment,including the basement membranes(BMs),is dynamically remodeled.However,whether and how ECM regulates tumor glycolysis is largely unknown.We show that type IV collagens,components of BMs essential for the tissue integrity and proper function,are differentially expressed in breast cancer subtypes thatα5 chain(α5(IV))is preferentially expressed in the luminal-type breast cancer and is regulated by estrogen receptor-α.α5(IV)is indispensable for luminal breast cancer development.Ablation ofα5(IV)significantly reduces the growth of luminal-type breast cancer cells and impedes the development of luminal-type breast cancer.Impaired cell growth and tumor development capability ofα5(IV)-ablated luminal breast cancer cells is attributed to the reduced expression of glucose transporter and glycolytic enzymes and impaired glycolysis in luminal breast cancer cells.Non-integrin collagen receptor discoidin domain receptor-1(DDR1)expression and p38 mitogen-activated protein kinase activation are attenuated inα5(IV)-ablated luminal breast cancer cells,resulting in reduced c-Myc oncogene expression and phosphorylation.Ectopic expression of constitutively active DDR1 or c-Myc restores the expression of glucose transporter and glycolytic enzymes,and thereafter restores aerobic glycolysis,cell proliferation,and tumor growth of luminal breast cancer.Thus,type IV collagenα5 chain is a luminal-type breast cancer-specific microenvironmental regulator modulating cancer cell metabolism. | Yuexin Wu Xiangming Liu Yue Zhu Yuemei Qiao Yuan Gao Jianfeng Chen Gaoxiang Ge | 2022 | Journal of Molecular Cell Biology2022，14，10： | 0 |
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