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| 1 | Regulation of sister chromatid cohesion by nuclear PD-L1显示文摘Programmed death ligand-1(PD-L1 or B7-H1)is well known for its role in immune checkpoint regulation,but its function inside the tumor cells has rarely been explored.Here we report that nuclear PD-L1 is important for cancer cell sister chromatid cohesion.We found that depletion of PD-L1 suppresses cancer cell proliferation,colony formation in vitro,and tumor growth in vivo in immune-deficient NSG mice independent of its role in immune checkpoint.Specifically,PD-L1 functions as a subunit of the cohesin complex,and its deficiency leads to formation of multinucleated cells and causes a defect in sister chromatid cohesion.Mechanistically,PD-L1 compensates for the loss of Sororin,whose expression is suppressed in cancer cells overexpressing PD-L1.PD-L1 competes with Wing Apart-Like(WAPL)for binding to PDS5B,and secures proper sister chromatid cohesion and segregation.Our findings suggest an important role for nuclear PD-L1 in cancer cells independent of its function in immune checkpoint. | Jia Yu Bo Qin Ann MMoyer Somaira Nowsheen Xinyi Tu Haidong Dong Judy CBoughey Matthew PGoetz Richard Weinshilboum Zhenkun Lou Liewei Wang | 2020 | Cell Research2020，30，7： | 3 |
| 2 | SARS-CoV-2 non-structural protein 13 (nspl3) hijacks host deubiquitinase USP13 and counteracts host antiviral immune response显示文摘Dear Editor,COVID-19(Coronavirus Disease-2019),a respiratory disease caused by the novel virus strain,SARS-CoV-2(severe acute respiratory syndrome coronavirus 2),an enveloped,positive-sense,single-stranded RNA betacoronavirus of the family Corona-viridae,has spread worldwide.1 Notably,SARS-CoV-2 infection led to poor induction of typeⅠ interferon response,and the impaired type Ⅰ IFN responses have been shown to be associated with severe COVID-19 disease.2 However,molecular mechanisms by which SARS-CoV-2 suppresses type Ⅰ IFN production,and how host cells respond to the inhibition of type Ⅰ IFN response during SARS-CoV-2 infection,remain largely unknown. | Guijie Guo Ming Gao Xiaochen Gao Bibo Zhu Jinzhou Huang Kuntian Luo Yong Zhang Jie Sun Min Deng Zhenkun Lou | 2021 | Signal Transduction and Targeted Therapy2021，6，4： | 2 |
| 3 | DBC1 Functions as a Tumor Suppressor by Regulating p53 Stability显示文摘 | Bo Qin Katherine Minter-Dykhouse Jia Yu Jun Zhang Tongzheng Liu Haoxing Zhang SeungBaek Lee JungJin Kim Liewei Wang Zhenkun Lou | 2015 | Cell Reports2015，，： | 1 |
| 4 | WSB1 overcomes oncogene-induced senescence by targeting ATM for degradation显示文摘导致 Oncogene 的老朽(OIS ) 或通过 DNA 损坏反应的 apoptosis 是 tumorigenesis 的一个重要障碍。克服这个障碍导致反常房间增长, genomic 不稳定性,和细胞的转变,并且最后允许癌症发展。然而, OIS 障碍怎么被克服,仍然保持不清楚。这里,我们证明 E3 ubiquitin ligase WD 重复并且 SOCS 包含盒子的蛋白质(WSB1 ) 1 在克服 OIS 起一个作用。在主要房间的 WSB1 表示帮助 OIS 的 bypass,导致反常增长和细胞的转变。机械学地, WSB1 支持 ATM ubiquitination,导致从 OIS 的 ATM 降级和逃跑。而且,我们作为 WSB1 的在上游的 kinase 识别 CDK。调停 CDK 的 phosphorylation 由支持它的 monomerization 激活 WSB1。在人的癌症织物并且在 vitro 模型,导致 WSB1 的 ATM 降级在 tumorigenic 前进期间是一个早事件。我们建议 WSB1 是通过 ATM 降级和 tumorigenesis 障碍的破坏的早 oncogenic 事件的关键播放器之一。我们的工作在 premalignant 损害建立癌症开发和前进的重要机制。 | Jung Jin Kim Seung Baek Lee Sang-Yeop Yi Sang-Ah Han Sun-Hyun Kim Jong-Min Lee Seo-Yun Tong Ping Yin Bowen Gao Jun Zhang Zhenkun Lou | 2017 | Cell Research2017，27，2： | 1 |
| 5 | FKBP51 Affects Cancer Cell Response to Chemotherapy by Negatively Regulating Akt显示文摘 | Huadong Pei Liang Li Brooke L. Fridley Gregory D. Jenkins Krishna R. Kalari Wilma Lingle Gloria Petersen Zhenkun Lou Liewei Wang | 2009 | Cancer Cell2009，，3： | 1 |
| 6 | A general method for growth of perovskite single-crystal arrays for high performance photodetectors显示文摘Perovskite single-crystal arrays have attracted intensive attention because of their great potentials for integrated optoelectronic devices.However,the traditional top-down lithography strategy requires complex processing and is detrimental to perovskite crystal structures,which is incompatible to directly pattern perovskite single crystals.Herein,we report a lithography-free method to realize the controllable growth of perovskite single-crystal arrays.Through introducing a printed hydrophilic-hydrophobic substrate into the crystallization system,the MAPbCl_(3) single-crystal arrays with precise location and uniform size are effectively fabricated.This method can be applied to prepare diverse perovskite single-crystal arrays,including MAPbBr_(3),CsPbCl_(3),CsPbBr_(3),Cs_(3)Cu_(2)I_(5),Cs_(3)Bi_(2)I_(9),and(BA)_(2)(MA)_(3)Pb_(4)I_(11).The perovskite single crystals can be selectively grown on the electrodes to fabricate ultraviolet photodetectors.The strategy demonstrates a facile approach to fabricate large-scale perovskite single-crystal arrays and opens a pathway to produce diverse perovskite optoelectronic devices. | Shiheng Wang Zhenkun Gu Rudai Zhao Ting Zhang Yunjie Lou Lutong Guo Meng Su Lihong Li Yiqiang Zhang Yanlin Song | 2022 | Nano Research2022，15，7： | 0 |
| 7 | A ribosomal gene panel predicting a novel synthetic lethality in non-BRCAness tumors显示文摘Poly(ADP-ribose)polymerase(PARP)inhibitors are one of the most exciting classes of targeted therapy agents for cancers with homologous recombination(HR)deficiency.However,many patients without apparent HR defects also respond well to PARP inhibitors/cisplatin.The biomarker responsible for this mechanism remains unclear.Here,we identified a set of ribosomal genes that predict response to PARP inhibitors/cisplatin in HR-proficient patients.PARP inhibitor/cisplatin selectively eliminates cells with high expression of the eight genes in the identified panel via DNA damage(ATM)signaling-induced pro-apoptotic ribosomal stress,which along with ATM signaling-induced pro-survival HR repair constitutes a new model to balance the cell fate in response to DNA damage.Therefore,the combined examination of the gene panel along with HR status would allow for more precise predictions of clinical response to PARP inhibitor/cisplatin.The gene panel as an independent biomarker was validated by multiple published clinical datasets,as well as by an ovarian cancer organoids library we established.More importantly,its predictive value was further verified in a cohort of PARP inhibitor-treated ovarian cancer patients with both RNA-seq and WGS data.Furthermore,we identified several marketed drugs capable of upregulating the expression of the genes in the panel without causing HR deficiency in PARP inhibitor/cisplatin-resistant cell lines.These drugs enhance PARP inhibitor/cisplatin sensitivity in both intrinsically resistant organoids and cell lines with acquired resistance.Together,our study identifies a marker gene panel for HR-proficient patients and reveals a broader application of PARP inhibitor/cisplatin in cancer therapy. | Chao Zhang Qiang Guo Lifeng Chen Zheming Wu Xiao-Jian Yan Chengyang Zou Qiuxue Zhang Jiahong Tan Tian Fang Qunxian Rao Yang Li Shizhen Shen Min Deng Liewei Wang Huanyao Gao Jia Yu Hu Li Cheng Zhang Somaira Nowsheen Jake Kloeber Fei Zhao Ping Yin Chunbo Teng Zhongqiu Lin Kun Song Shuzhong Yao Liangqing Yao Lingying Wu Yong Zhang Xiaodong Cheng Qinglei Gao Jian Yuan Zhenkun Lou Jin-San Zhang | 2023 | Signal Transduction and Targeted Therapy2023，8，6： | 0 |
| 8 | FGF10 mitigates doxorubicin-induced myocardial toxicity in mice via activation of FGFR2b/PHLDA1/AKT axis显示文摘Doxorubicin is a common chemotherapeutic agent in clinic, but myocardial toxicity limits its use. Fibroblast growth factor (FGF) 10, a multifunctional paracrine growth factor, plays diverse roles in embryonic and postnatal heart development as well as in cardiac regeneration and repair. In this study we investigated the role of FGF10 as a potential modulator of doxorubicin-induced cardiac cytotoxicity and the underlying molecular mechanisms. Fgf10+/− mice and an inducible dominant negative FGFR2b transgenic mouse model (Rosa26rtTA;tet(O)sFgfr2b) were used to determine the effect of Fgf10 hypomorph or blocking of endogenous FGFR2b ligands activity on doxorubicin-induced myocardial injury. Acute myocardial injury was induced by a single injection of doxorubicin (25 mg/kg, i.p.). Then cardiac function was evaluated using echocardiography, and DNA damage, oxidative stress and apoptosis in cardiac tissue were assessed. We showed that doxorubicin treatment markedly decreased the expression of FGFR2b ligands including FGF10 in cardiac tissue of wild type mice, whereas Fgf10+/− mice exhibited a greater degree of oxidative stress, DNA damage and apoptosis as compared with the Fgf10+/+ control. Pre-treatment with recombinant FGF10 protein significantly attenuated doxorubicin-induced oxidative stress, DNA damage and apoptosis both in doxorubicin-treated mice and in doxorubicin-treated HL-1 cells and NRCMs. We demonstrated that FGF10 protected against doxorubicin-induced myocardial toxicity via activation of FGFR2/Pleckstrin homology-like domain family A member 1 (PHLDA1)/Akt axis. Overall, our results unveil a potent protective effect of FGF10 against doxorubicin-induced myocardial injury and identify FGFR2b/PHLDA1/Akt axis as a potential therapeutic target for patients receiving doxorubicin treatment. | De-pu Zhou Lian-cheng Deng Xiao Feng Hui-jing Xu Ye Tian Wei-wei Yang Ping-ping Zeng Li-hui Zou Xi-hua Yan Xia-yan Zhu Dan-hua Shu Qiang Guo Xiao-ying Huang Saverio Bellusci Zhenkun Lou Xiao-kun Li Jin-San Zhang | 2023 | Acta Pharmacologica Sinica2023，44，10： | 0 |
| 9 | Author Correction:Regulation of sister chromatid cohesion by nuclear PD-L1显示文摘In the initial version of this article published online,there was a typo of the figure number in the discussion section.'Fig.4a,b' should be 'Fig.5a,b'.The correct information is as follows.This correction does not affect the description of the results or the conclusion of this work. | Jia Yu Bo Qin Ann M.Moyer Somaira Nowsheen Xinyi Tu Haidong Dong Judy C.Boughey Matthew P.Goetz Richard Weinshilboum Zhenkun Lou Liewei Wang | 2020 | Cell Research2020，30，9： | 0 |
| 10 | Regulation of AMPK activation by extracellular matrix stiffness in pancreatic cancer显示文摘The adenosine monophosphate(AMP)-activated protein kinase(AMPK)sits at a cen-tral node in the regulation of energy metabolism and tumor progression.AMPK is best known to sense high cellular ADP or AMP levels,which indicate the depletion of energy stores.Previous studies have shown that the low expression of phosphorylated AMPK is associated with a poor prognosis of pancreatic cancer.In this study,we report that AMPK is also highly sensitive to extracellular matrix(ECM)stiffness.We found that AMPK is activated in cells when cultured under low ECM stiffness conditions and is functionally required for the metabolic switch induced by ECM stiffness.This regulation of AMPK requires the Hippo kinases but not LKB1/CaMKKp.Hippo kinases directly phosphorylate AMPKa at Thr172 to activate AMPK at low ECM stiffness.Furthermore,we found AMPK activity is inhibited in patients with pancreatic ductal adenocarcinoma(PDAC)with high ECM stiffness and is associated with a poor survival outcome.The activation of Hippo kinases by ROCK inhibitor Y-27632 in combination with the mitochondrial inhibitor metformin synergistically activates AMPK and dramatically inhibits PDAC growth.Together,these findings establish a novel model for AMPK regulation by the mechanical properties of ECMs and provide a rationale for simultaneously targeting the ECM stiffness-Hippo kinases-AMPK signaling and low glucose-LKB1-AMPK signaling pathways as an effective therapeutic strategy against PDAC. | Xin Xu Yuan Fang Somaira Nowsheen Ye-Xiong Li Zhenkun Lou Min Deng | 2024 | Genes & Diseases2024，11，3： | 0 |
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