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  • The expanding role for small molecules in immuno-oncology

    Nature Reviews Drug Discovery | 2022 | 查看原文 |

    作者：Rienk Offringa, Lisa K?tzner, Bayard Huck & Klaus Urbahns

    摘要：The advent of immune checkpoint inhibition (ICI) using antibodies against PD1 and its ligand PDL1 has prompted substantial efforts to develop complementary drugs. Although many of these are antibodies directed against additional checkpoint proteins, there is an increasing interest in small-molecule immuno-oncology drugs that address intracellular pathways, some of which have recently entered clinical trials. In parallel, small molecules that target pro-tumorigenic pathways in cancer cells and the tumour microenvironment have been found to have immunostimulatory effects that synergize with the action of ICI antibodies, leading to the approval of an increasing number of regimens that combine such drugs. Combinations with small molecules targeting cancermetabolism, cytokine/chemokine and innate immune pathways, and T cell checkpoints are now under investigation. This Review discusses the recent milestones and hurdles encountered in this area of drug development, as well as our views on the best path forward.
    展開

    關(guān)鍵詞：PD1/PDL1，免疫檢查點(diǎn)，癌癥代謝、細(xì)胞因子/趨化因子，先天免疫，腫瘤微環(huán)境

    應(yīng)用產(chǎn)品：Lumit? HMGB1 Human/Mouse ImmunoassayLumit? HMGB1 Human/Mouse ImmunoassayRealTime-Glo? Extracellular ATP AssayGlutamine/Glutamate-Glo? Assay

  • Interactions of WRKY15 and WRKY33 transcription factors and their roles in the resistance of oilseed rape to Sclerotinia infection

    Plant Biotechnology Journal | 2018 | 查看原文 |

    作者：Fei Liu,Xiaoxia Li,Meirong Wang,Jing Wen,Bin Yi,Jinxiong Shen,Chaozhi Ma,Tingdong Fu,Jinxing Tu

    摘要：WRKY transcription factors are known to participate in the defence responses of higher plants. However, little is known about the roles of such proteins, especially regarding their functions in the resistance of oilseed rape (Brassica napus) to Sclerotinia sclerotiorum, a necrotrophic fungal pathogen that causes stem rot. In this study, we identified BnWRKY33 as a S. sclerotiorum-responsive gene that positively regulates resistance to this pathogen by enhancing the expression of genes involved in camalexin synthesis and genes regulated by salicylic acid (SA) and jasmonic acid (JA). We also identified a S. sclerotiorum-responsive region in the promoter of BnWRKY33, which we revealed to be a relatively conserved W-box region in the promoters of homologous genes in different species. Using this S. sclerotiorum-responsive region as bait in a yeast one-hybrid assay, we identified another WRKY transcription factor, BnWRKY15, and observed that both BnWRKY15 and BnWRKY33 could bind to this region. In addition, BnWRKY15 overexpression simultaneously increased the susceptibility of B. napus to S. sclerotiorum and down-regulated BnWRKY33 after different durations of infection. Furthermore, BnWRKY15, which contains a transcriptional repression domain, exhibited reduced transactivation ability and could reduce the transactivation ability of BnWRKY33 in Arabidopsis protoplast assays. Therefore, we suggest that the increased susceptibility of BnWRKY15-overexpressing plants results from reduced BnWRKY33 expression, which is due to the inhibition of BnWRKY33 transcriptional activation by BnWRKY15.
    展開

    關(guān)鍵詞：WRKY轉(zhuǎn)錄因子，轉(zhuǎn)錄激活，病原體抗性，W-box區(qū)域，植物易感性研究

    應(yīng)用產(chǎn)品：Dual-Luciferase? Reporter Assay System

  • Fine-Tuning of Cholesterol Homeostasis Controls Erythroid Differentiation

    Advanced Science | 2021 | 查看原文 |

    作者：Zhiyuan Lu, Lixia Huang, Yanxia Li, Yan Xu, Ruihao Zhang, Qian Zhou, Qi Sun, Yi Lu, Junjie Chen, Yuemao Shen, Jian Li, Baobing Zhao

    摘要：Lipid metabolism is essential for stemness maintenance, self-renewal, and differentiation of stem cells, however, the regulatory function of cholesterol metabolism in erythroid differentiation is poorly studied. In the present study, a critical role for cholesterol homeostasis in terminal erythropoiesis is uncovered. The master transcriptional factor GATA1 binds to Sterol-regulatory element binding protein 2 (SREBP2) to downregulate cholesterol biosynthesis, leading to a gradual reduction in intracellular cholesterol levels. It is further shown that reduced cholesterol functions to block erythroid proliferation via the cholesterol/mTORC1/ribosome biogenesis axis, which coordinates cell cycle exit in the late stages of erythroid differentiation. The interaction of GATA1 and SREBP2 also provides a feedback loop for regulating globin expression through the transcriptional control of NFE2 by SREBP2. Importantly, it is shown that disrupting intracellular cholesterol hemostasis resulted in defect of terminal erythroid differentiation in vivo. These findings demonstrate that fine-tuning of cholesterol homeostasis emerges as a key mechanism for regulating erythropoiesis.
    展開

    關(guān)鍵詞：GATA1，SREBP2，膽固醇平衡，去核，紅細(xì)胞生成， 核糖體合成

    應(yīng)用產(chǎn)品：Dual-Glo? Luciferase Assay System

  • KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling

    Nature Communications | 2022 | 查看原文 |

    作者：Bo Yu, Jun Su, Qiqi Shi, Qing Liu, Jun Ma, Guoqing Ru, Lei Zhang, Jian Zhang, Xichun Hu, Jianming Tang

    摘要：Smad nuclear-interacting protein 1 (SNIP1) is a transcription repressor related to the TGF-β signaling pathway and associates with c-MYC, a key regulator of cell proliferation and tumor development. Currently, the mechanism by which SNIP1 regulates tumorigenesis and cancer metastasis is unknown. Here, we identify that SNIP1 is a non-histone substrate of lysine methyltransferase KMT5A, which undergoes KMT5A-mediated mono-methylation to promote breast cancer cell growth, invasion and lung metastasis. Mechanistically, we show KMT5A-mediated K301 methylation of SNIP1 represents a sensing signal to release histone acetyltransferase KAT2A and promotes the interaction of c-MYC and KAT2A, and the recruitment of c-MYC/KAT2A complex to promoter of c-MYC targets. This event ultimately inhibits the Hippo kinase cascade to enhance triple-negative breast cancer (TNBC) metastasis by transcriptionally activating MARK4. Co-inhibition of KMT5A catalytic activity and YAP in TNBC xenograft-bearing animals attenuates breast cancer metastasis and increases survival. Collectively, this study presents an KMT5A methylation-dependent regulatory mechanism governing oncogenic function of SNIP1.
    展開

    關(guān)鍵詞：Smad核相互作用蛋白1（SNIP1），TGF-β信號(hào)通路，乳腺癌，甲基化

    應(yīng)用產(chǎn)品：Dual-Luciferase? Reporter Assay System

  • Increasing the efficiency and targeting range of cytidine base editors through fusion of a single-stranded DNA-binding protein domain

    Nature Cell Biology | 2020 | 查看原文 |

    作者：Xiaohui Zhang, Liang Chen, Biyun Zhu, Liren Wang, Caiyu Chen, Mengjia Hong, Yifan Huang, Huiying Li, Honghui Han, Bailian Cai, Weishi Yu, Shuming Yin, Lei Yang, Zuozhen Yang, Meizhen Li

    摘要：Cytidine base editors are powerful genetic tools that catalyse cytidine to thymidine conversion at specific genomic loci, and further improvement of the editing range and efficiency is critical for their broader applications. Through insertion of a non-sequence-specific single-stranded DNA-binding domain from Rad51 protein between Cas9 nickase and the deaminases, serial hyper cytidine base editors were generated with substantially increased activity and an expanded editing window towards the protospacer adjacent motif in both cell lines and mouse embryos. Additionally, hyeA3A-BE4max selectively catalysed cytidine conversion in TC motifs with a broader editing range and much higher activity (up to 257-fold) compared with eA3A-BE4max. Moreover, hyeA3A-BE4max specifically generated a C-to-T conversion without inducing bystander mutations in the haemoglobin gamma gene promoter to mimic a naturally occurring genetic variant for amelioration of β-haemoglobinopathy, suggesting the therapeutic potential of the improved base editors.
    展開

    關(guān)鍵詞：基因編輯，遺傳變異，β-血紅蛋白病，胞嘧啶堿基編輯器

    應(yīng)用產(chǎn)品：CellTiter 96? AQueous One Solution Cell Proliferation Assay (MTS)

  • The IKKβ-USP30-ACLY Axis Controls Lipogenesis and Tumorigenesis

    Hepatology | 2021 | 查看原文 |

    作者：Li Gu,Yahui Zhu,Xi Lin,Bingjun Lu,Xinyi Zhou,Feng Zhou,Qiu Zhao,Edward V. Prochownik,Youjun Li

    摘要：Background and AimsHepatocellular carcinoma (HCC) is a leading cause of cancer-related death that develops as a consequence of obesity, cirrhosis, and chronic hepatitis. However, the pathways along which these changes occur remain incompletely understood.Approach and ResultsIn this study, we show that the deubiquitinase USP30 is abundant in HCCs that arise in mice maintained on high-fat diets. IKKβ phosphorylated and stabilized USP30, which promoted USP30 to deubiquitinate ATP citrate lyase (ACLY) and fatty acid synthase (FASN). IKKβ also directly phosphorylated ACLY and facilitated the interaction between USP30 and ACLY and the latter’s deubiquitination. In HCCs arising in DEN/CCl4-treated mice, USP30 deletion attenuated lipogenesis, inflammation, and tumorigenesis regardless of diet. The combination of ACLY inhibitor and programmed death ligand 1 antibody largely suppressed chemical-induced hepatocarcinogenesis. The IKKβ-USP30-ACLY axis was also found to be up-regulated in human HCCs.ConclusionsThis study identifies an IKKβ-USP30-ACLY axis that plays an essential and wide-spread role in tumor metabolism and may be a potential therapeutic target in HCC.
    展開

    關(guān)鍵詞：肝細(xì)胞癌(HCC)，去泛素酶USP30，IKKβ磷酸化，IKKβ-USP30-ACLY，腫瘤代謝

    應(yīng)用產(chǎn)品：

  • A novel histone H4 variant H4G regulates rDNA transcription in breast cancer

    Nucleic Acids Research | 2019 | 查看原文 |

    作者：Mengping Long, Xulun Sun, Wenjin Shi, An Yanru, Sophia T C Leung, Dongbo Ding, Manjinder S Cheema, Nicol MacPherson, Christopher J Nelson, Juan Ausio, Yan Yan, Toyotaka Ishibashi

    摘要：Histone variants, present in various cell types and tissues, are known to exhibit different functions. For example, histone H3.3 and H2A.Z are both involved in gene expression regulation, whereas H2A.X is a specific variant that responds to DNA double-strand breaks. In this study, we characterized H4G, a novel hominidae-specific histone H4 variant. We found that H4G is expressed in a variety of human cell lines and exhibit tumor-stage dependent overexpression in tissues from breast cancer patients. We found that H4G localized primarily to the nucleoli of the cell nucleus. This localization was controlled by the interaction of the alpha-helix 3 of the histone fold motif with a histone chaperone, nucleophosmin 1. In addition, we found that modulating H4G expression affects rRNA expression levels, protein synthesis rates and cell-cycle progression. Our data suggest that H4G expression alters nucleolar chromatin in a way that enhances rDNA transcription in breast cancer tissues.
    展開

    關(guān)鍵詞：組蛋白變體，H3.3，H2A.Z，乳腺癌，rRNA表達(dá)、蛋白質(zhì)合成，細(xì)胞周期

    應(yīng)用產(chǎn)品：FuGENE? HD Transfection Reagent

  • Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly

    Nature communications | 2020 | 查看原文 |

    作者：Yuying Li, Jie Yuan, Fengyuan Chen, Suyang Zhang, Yu Zhao, Xiaona Chen, Leina Lu, Liang Zhou, Ching Yan Chu, Hao Sun & Huating Wang

    摘要：The functional study of lncRNAs in skeletal muscle satellite cells (SCs) remains at the infancy stage. Here we identify SAM (Sugt1 asssociated muscle) lncRNA that is enriched in the proliferating myoblasts. Global deletion of SAM has no overt effect on mice but impairs adult muscle regeneration following acute damage; it also exacerbates the chronic injury-induced dystrophic phenotype in mdx mice. Consistently, inducible deletion of SAM in SCs leads to deficiency in muscle regeneration. Further examination reveals that SAM loss results in a cell-autonomous defect in the proliferative expansion of myoblasts. Mechanistically, we find SAM interacts and stabilizes Sugt1, a co-chaperon protein key to kinetochore assembly during cell division. Loss of SAM or Sugt1 both disrupts kinetochore assembly in mitotic cells due to the mislocalization of two components: Dsn1 and Hec1. Altogether, our findings identify SAM as a regulator of SC proliferation through facilitating Sugt1 mediated kinetochore assembly during cell division.
    展開

    關(guān)鍵詞：lncRNA，SAM，有絲分裂細(xì)胞，著絲粒組裝，骨骼肌衛(wèi)星細(xì)胞增殖

    應(yīng)用產(chǎn)品：CellTiter 96? AQueous One Solution Cell Proliferation Assay (MTS)

  • Sperm associated antigen 4 promotes SREBP1-mediated de novo lipogenesis via interaction with lamin A/C and contributes to tumor progression in hepatocellular carcinoma

    Cancer letters | 2022 | 查看原文 |

    作者：Tengfei Liu, Junming Yu, Chao Ge, Fangyu Zhao, Jing Chen, Chunxiao Miao, Wenjiao Jin, Qingqing Zhou, Qin Geng, Hechun Lin, Hua Tian, Taoyang Chen, Haiyang Xie, Ying Cui, Ming Yao,

    摘要：Hepatocellular carcinoma (HCC) is a highly malignant tumor and its progression is associated with altered lipid metabolism in precancerous lesions, such as non-alcoholic fatty liver disease. Here, we identified sperm associated antigen 4 (SPAG4), and explored its oncogenic role in HCC progression. Database analysis and immunohistochemistry indicated increased level of SPAG4 in HCC tissues which was of prognostic value. Gain/loss-of-function experiments showed that SPAG4 exerted oncogenic roles in HCC growth both in vitro and in vivo. RNA sequencing revealed activation of a lipogenic state and SREBP1-mediated pathway following SPAG4 overexpression. Mechanistically, the N-terminal region of SPAG4 bound to lamin A/C, which increased SREBP1 expression, nuclear translocation, and transcriptional activity. Treatment with orlistat, a lipid synthesis inhibitor, reversed SPAG4-mediated oncogenic effects, and its efficacy varied with SPAG4 level. The effect of orlistat was further amplified when combined with sorafenib in tumor xenograft mouse models. Our study provides evidence that SPAG4 mediates HCC progression by affecting lipid metabolism. Administration of orlistat combined with sorafenib reverses SPAG4-mediated oncogenesis in HCC cells and ectopic xenograft tumors in mice, suggesting that this pathway represents a potential target for HCC treatment.
    展開

    關(guān)鍵詞：肝細(xì)胞性肝癌，核纖層蛋白，Lamin A/C，脂肪生成，SPAG4，SREBP1

    應(yīng)用產(chǎn)品：

  • Alpk1 Sensitizes Pancreatic Beta Cells to Cytokine-Induced Apoptosis via Upregulating TNF-α Signaling Pathway

    Front Immunol | 2021 | 查看原文 |

    作者：Fei Ding, Xi Luo, Yiting Tu, Xianlan Duan, Jia Liu, Lijing Jia, Peilin Zheng

    摘要：Pancreatic beta cell failure is the hallmark of type 1 diabetes (T1D). Recent studies have suggested that pathogen recognizing receptors (PRRs) are involved in the survival, proliferation and function of pancreatic beta cells. So far, little is known about the role of alpha-protein kinase 1 (ALPK1), a newly identified cytosolic PRR specific for ADP-β-D-manno-heptose (ADP-heptose), in beta cell survival. In current study we aimed to fill the knowledge gap by investigating the role of Alpk1 in the apoptosis of MIN6 cells, a murine pancreatic beta cell line. We found that the expression of Alpk1 was significantly elevated in MIN6 cells exposed to pro-inflammatory cytokines, but not to streptozotocin, low-dose or high-dose glucose. Activation of Alpk1 by ADP heptose alone was insufficient to induce beta cell apoptosis. However, it significantly exacerbated cytokine-induced apoptosis in MIN6 cells. Mechanistic investigations showed that Alpk1 activation was potent to further induce the expression of tumor necrosis factor (TNF)-α and Fas after cytokine stimulation, possibly due to enhanced activation of the TIFA/TAK1/NF-κB signaling axis. Treatment of GLP-1 receptor agonist decreased the expression of TNF-α and Fas and improved the survival of beta cells exposed to pro-inflammatory cytokines and ADP heptose. In summary, our data suggest that Alpk1 sensitizes beta cells to cytokine-induced apoptosis by potentiating TNF-α signaling pathway, which may provide novel insight into beta cell failure and T1D development.
    展開

    關(guān)鍵詞：Alpk1,TNF-α信號(hào)，細(xì)胞凋亡，胰島β細(xì)胞，促炎細(xì)胞因子

    應(yīng)用產(chǎn)品：CellTox? Green Cytotoxicity Assay

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