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  • PROJ Verstraetearchaea LWZ-6

    Kejia Wu, Biogas Institute of Ministry of Agriculture and Rural Affairs,2022.11.10

    Description

    A highly enriched microbial consortium from Shengli oil field sludge, containing a single archaeal species belonging to the phylum Verstraetearchaeota. The Verstraetearchaea LWZ-6 is a heterotrophic methanogen that utilizes methanol or monomethylamine as electron acceptors and hydrogen as electron donor.

    OEP003742

  • PROJ PDK4-dependent hypercatabolism and lactate production of senescence cells promotes cancer malignancy

    Yu Sun, Shanghai Institute of Nutrition and Health, CAS,2023.12.28

    Description

    Technical advances in next generation sequencing (NGS) has revolutionized system-based analysis of genome-wide expression, cellular pathways and responses. We performed this study to establish the transcriptomic profiles of human prostate cancer cell lines exposed to conditioned media from human primary stromal cells engineered to express pyruvate dehydrogenase kinase 4 (PDK4), a key enzyme that is correlated with glucose metabolism, negatively regulates the conversion of pyruvate to acetyl-CoA and plays important roles in cancer progression and multiple other pathological events.

    OEP004913

  • PROJ ARID2 mitigates hepatic steatosis via promoting the ubiquitination of JAK2 (house mouse)

    Jingjing Li, Shanghai Institute of Nutrition and Health, CAS,2023.12.27

    Description

    Non-alcoholic fatty liver disease (NAFLD) has become a growing public health problem. However, the complicated pathogenesis of NAFLD contributes to the deficiency of effective clinical treatment. Here, we elucidated that liver-specific loss of Arid2 induced hepatic steatosis and this progression could be exacerbated by HFD. Mechanistic study revealed that ARID2 repressed JAK2-STAT5-PPARγ signaling pathway by promoting the ubiquitination of JAK2, which was mediated by NEDD4L, a novel E3 ligase for JAK2. ChIP assay revealed that ARID2 recruited CARM1 to increase H3R17me2 level at NEDD4L promoter and activated the transcription of NEDD4L. Moreover, inhibition of Jak2 by Fedratinib in liver-specific Arid2 knockout mice alleviated HFD-induced hepatic steatosis. Downregulation of ARID2 and the reverse correlation between ARID2 and JAK2 were also observed in clinical samples. Therefore, our study has revealed an important role of ARID2 in the development of NAFLD and provides a potential therapeutic strategy for NAFLD. Overall design: Comparative gene expression profiling analysis of RNA-seq data for livers of Arid2 WT and LKO mice.

    OEP004908

  • PROJ PPDPF suppresses the development of hepatocellular carcinoma through TRIM21-mediated ubiquitination of RIPK1

    Jingjing Li, Shanghai Institute of Nutrition and Health, CAS,2023.12.27

    Description

    Pancreatic progenitor cell differentiation and proliferation factor (PPDPF) has been reported to play a role in tumorigenesis. However, its function in hepatocellular carcinoma (HCC) remains poorly understood. In this study, we report that PPDPF is significantly downregulated in HCC and indicats poor prognosis and survival for HCC patients. In the DEN-induced HCC mouse model, hepatocyte-specific depletion of Ppdpf promots hepatocarcinogenesis, and reintroduction of PPDPF into LKO mice inhibits the accelerated HCC development. Mechanistic study reveals that PPDPF regulated NF-kB signaling through modulation of RIPK1 ubiquitination. PPDPF interacts with RIPK1 and facilitates K63-linked ubiquitination of RIPK1 via recruiting the E3 ligase TRIM21, which catalyzs K63-linked ubiquitination of RIPK1 on K140. In addition, liver-specific overexpression of PPDPF activats NF-kB signaling, attenuats apoptosis and compensatory proliferation in mice, which significantly suppresses HCC development. This work identifies PPDPF as a regulator of NF-kB signaling and provides a potential therapeutic candidate for HCC.

    OEP004906

  • PROJ Transcriptomic profiling of senescent human stromal cells upon medicinal intervention with rutin (human)

    Yu Sun, Shanghai Institute of Nutrition and Health, CAS,2023.12.27

    Description

    Aging and age-related pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using natural or synthetic agents would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of rutin, a bioactive phytochemical component derived from natural plants specifically ginkgo boliva, in targeting senescent cells via suppression of the SASP. This study demonstrates the efficacy of rutin as medicinal agent in controlling the influence of senescent human stromal cells and provides a strong rationale for its future use in aging intervention and geriatric medicine. Overall design: Examination of in vitro efficacy of rutin, a polyphenolic compound in treating human senescent stromal cells (PSC27 line). Ginkgo biloba products are widely consumed herbal supplements that contain ingredients with anti-oxidant potentials. However, the active agents in ginkgo biloba extracts (GBE) remain unclear, and its major ingredients such as rutin has not been extensively investigated in cellular senescence. This assay was performed beyond previous studies reporting the effects of GBE in anti-diabetic, anti-cataract therapy, anti-inflammation and anti-tumor therapies.

    OEP004909

  • PROJ Targeting UHRF1-SAP30-MXD4 axis for leukemia initiating cell eradication in myeloid leukemia

    Wang lan, Shanghai Institute of Nutrition and Health,2023.12.11

    Description

    Aberrant self-renewal of leukemia initiation cells (LICs) drives aggressive acute myeloid leukemia (AML). Here, we report that UHRF1, an epigenetic regulator that recruits DNMT1 to methylate DNA, is highly expressed in AML and predicts poor prognosis. UHRF1 is required for myeloid leukemogenesis by maintaining self-renewal of LICs. Mechanistically, UHRF1 directly interacts with Sin3A associated protein 30 (SAP30) through two amino acids, G572 and F573 in its SRA domain, to repress gene expression. Depletion of UHRF1 or SAP30 derepresses an important target gene, MXD4, which encodes a MYC antagonist, and leads to suppression of leukemogenesis. Knockdown of MXD4 can rescue the leukemogenesis by activating the MYC pathway. Lastly, we identified a UHRF1 inhibitor, UF146, and demonstrated its significant therapeutic efficacy in the myeloid leukemia PDX model. Taken together, these studies reveal the mechanisms for altered epigenetic programs in AML and provide a promising targeted therapeutic strategy against AML.

    OEP004818

  • PROJ Metatranscriptomic data in China Sea

    Jinxin Xu, Xiamen University,2023.03.12

    Description

    OEP004010

  • PROJ Loss of PTPRS Elicits Potent Metastatic Capability and Resistance to Temozolomide in Glioblastoma

    Lunshan Xu, Army Medical University Daping Hospital: Third Military Medical University Daping Hospital,2024.02.02

    Description

    Glioblastoma (GBM) is the most aggressive brain tumor type with worse clinical outcome, due to the hallmarks of strong invasiveness, high rate of recurrence and therapeutic resistance to temozolomide (TMZ), the first-line drug for GBM, representing a major challenge for successful GBM therapeutics. Understanding the underlying mechanisms that drive GBM progression will shed novel insight on therapeutic strategies. Receptor-type tyrosine-protein phosphatase S (PTPRS) is a frequently mutated gene in human cancers, including GBM. Its role in GBM has not yet clarified. Here, inactivating PTPRS mutation or deficiency were frequently found in GBM, and deficiency in PTPRS significantly induced defects in G2M checkpoint and limited GBM cells proliferation, leading to potent resistance to TMZ treatment in vitro and in vivo. Surprisingly, loss of PTPRS triggered an unexpected mesenchymal phenotype that markedly enhances migratory capabilities of GBM cells through upregulating numerous matrix metalloproteinases (MMPs) via MAPK-MEK-ERK signaling. Therefore, this work provides a therapeutic window for precisely excluding PTPRS-mutated patients that does not respond to TMZ.

    OEP005053

  • PROJ SCI ST

    Wang Zeqing, The Interdisciplinary Research Center on Biology and Chemistry,2022.07.07

    Description

    OEP003508

  • PROJ Prokaryotic community assembly patterns in Yangtze Estuary water column

    Yihua Sun, ,2020.03.22

    Description

    We addressed the microbial composition, community assembly, and nitrogen metabolism in the oxygen minimum zones (OMZs) in Yangtze Estuary water using 16S rRNA gene sequencing, modeling, and metagenomics analyses.

    OEP000802