Ye Li

Jiangnan University

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Co-Authors

Cuiqin Fan

Shandong University

Shu Yan Yu

Shandong University

Tian Lan

Shandong University

Wenjing Wang

Soochow University

Chunmei Wang

Northeast Agricultural University

Lei Tian

Yangtze University

Rui Gao

Chinese Research Academy of Environmental Sciences

Yuxi Wei

University of Electronic Science and Technology of China

Qingzhang Li

Northeast Agricultural University

Hui Zhang

Qilu Hospital of Shandong University

Cooperative Institutions

Chinese Academy of Medical Sciences & Peking Union Medical College

Guangxi Medical University

Sun Yat-sen University

Chinese Academy of Sciences

Fudan University

Southern Medical University

Wuhan University

Sichuan University

Roche (United States)

Huazhong University of Science and Technology

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EP11.01-08 GSDME-dependent Pyroptosis Affects the Prognosis and Response to Immunotherapy in Lung Adenocarcinoma

Journal of Thoracic Oncology (2023)

Pengfei Cao Guoqiang Zhu Ye Li Hua Huang Wu Dong

Pyroptosis

10.1016/j.jtho.2023.09.1158

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MicroRNA let-7c inhibits Bcl-xl expression and regulates ox-LDL-induced endothelial apoptosis

BMB Reports (2012)

Bing Qin Bo Xiao Desheng Liang Ye Li Ting Jiang

Endothelial cells (ECs) apoptosis induced by oxidized low-density lipoprotein (ox-LDL) is thought to play a critical role in atherosclerosis. MicroRNAs (miRNAs) are a class of noncoding RNAs that posttranscriptionally regulate the expression of genes involved in diverse cell functions, including differentiation, growth, proliferation, and apoptosis. MiRNA let-7 family is known to be involved in the regulation of cell apoptosis. However, the function of let-7 in ox-LDL induced ECs apoptosis and atherosclerosis is still unknown. Here, we show that let-7c expression was markedly up-regulated in ox-LDL induced apoptotic human umbilical cord vein endothelial cells (HUVECs). Let-7c over-expression enhanced apoptosis in ECs whereas inhibition of let-7c could partly alleviate apoptotic cell death mediated by ox-LDL. Searching for how let-7c affected apoptosis, we discovered that antiapoptotic protein Bcl-xl was a direct target of let-7c in ECs. Our data suggest that let-7c contributes to endothelial apoptosis through suppression of Bcl-xl.

10.5483/bmbrep.2012.45.8.033

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Citations (54)

Pharmacokinetics of Icosapent Ethyl: An Open‐Label, Multiple Oral Dose, Parallel Design Study in Healthy Chinese Subjects

Clinical Pharmacology in Drug Development (2022)

Fei Yuan Hui Li Mengjie Yang Weili Chen Hanjing Chen

Icosapent ethyl (IPE) is a high-purity prescription form of eicosapentaenoic acid (EPA) ethyl ester that has been approved to lower triglyceride levels in adult patients with severe (≥500 mg/dL) hypertriglyceridemia. Before this study, there were no pharmacokinetics (PK) or safety data in Chinese patients after receiving IPE. The purpose of this study was to evaluate the PK of EPA in plasma and red blood cells and safety after oral administration of IPE capsules for 28 consecutive days in healthy Chinese subjects. It was a randomized, open-label, parallel-designed multiple-dose, phase I study. Twenty-four subjects were enrolled and randomly assigned to 2 groups, including 6 men and 6 women in each group. Group A received IPE 2.0 g/day (1×1 g twice daily), and group B received IPE 4.0 g/day (2×1 g twice daily) with dosing after standard meals for 28 days. During the treatment period, PK samples were collected from all subjects before the morning dose on days 1, 14, 26, and 28. Following completion of the last study drug administration in the morning on day 28, an 18-day posttreatment PK sample collection period was followed. Twenty-four eligible subjects were enrolled in this study, and 1 subject withdrew from the study. The main PK parameters (baseline-corrected maximum observed plasma concentration and area under the plasma concentration-time curve during a dosing interval) of plasma total EPA, RBC EPA, and plasma unesterified EPA increased with dose. Chinese healthy subjects who took IPE capsules orally in the dose range of 2.0 to 4.0 g/day for 28 consecutive days were safe and tolerable.

10.1002/cpdd.1130

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MicroRNA-181a Inhibits Tumor Proliferation, Invasiveness, and Metastasis and Is Downregulated in Gastric Cancer

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics (2015)

Lin Feng Ye Li Shuai Yan Shaoping Liu Wenjun Qian

MicroRNAs (miRNAs) play crucial roles in the development and progression of human cancers, including gastric cancer. The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of gastric cancer. Here we show that miR-181a levels were significantly downregulated in gastric cancer tissues compared with the adjacent normal regions in 80 paired samples. Moreover, the lower levels of miR-181a were associated with the pM or pTNM stage in clinical gastric cancer patients. In addition, the ectopic expression of miR-181a in the gastric cancer cell line HGC-27 inhibited cell proliferation, cell migration, and invasion by directly interacting with the mRNA encoding the oncogenic factor Prox1. Taken together, our results indicate that miR-181a might act as a tumor suppressor in gastric cancer, which may provide a novel diagnostic and therapeutic option for human gastric cancer in the near future.

Ectopic expression

10.3727/096504014x14024160459203

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Citations (21)

Long Noncoding RNA LINC02453 Inhibits HIV‐1 Replication by Binding With SEC13 to Regulate the Viral Productive Cycle

Journal of Medical Virology (2024)

Chen Xiu Rongfeng Chen Liufang Wen Tongxue Qin Yinlu Liao

ABSTRACT Emerging evidence underscores the pivotal role of long noncoding RNAs (lncRNAs) as crucial regulators within the HIV life cycle. However, the precise functions and detailed mechanisms by which lncRNAs operate in HIV‐1 highly exposed but persistently seronegative (HESN) individuals remain currently unknown. Through RNA sequencing analysis of the HESN individual and the matched control, we identified potential lncRNAs. Then, we conducted validation experiments at the population level, while cellular models of HIV‐1 infection were constructed for functional experimental investigations in vitro. Subcellular localization of the identified lncRNA was determined, followed by an exploration of the specific regulatory mechanism underlying HIV resistance through some experiments, such as RNA pull‐down, western blot and Hirt assays. LncRNA LINC02453 is highly expressed in HESN. Moreover, LINC02453 is identified as a novel lncRNA associated with heightened resistance to HIV‐1. LINC02453 is predominantly localized in the nucleus and binds to SEC13, a component of the nuclear pore complex, leading to the inhibition of HIV‐1 replication by regulating key processes such as late reverse transcription, nuclear import, and DNA integration. Our findings suggest that LINC02453 may serve as a prospective target for the development of innovative anti‐HIV therapeutics.

Transcription

10.1002/jmv.70116

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Supplementary Data from Blocking Wnt/β-catenin Signal Amplifies Anti-PD-1 Therapeutic Efficacy by Inhibiting Tumor Growth, Migration, and Promoting Immune Infiltration in Glioblastomas

Hui Zhang Yongyan Bi Yuxi Wei Jiayang Liu Kudelaidi Kuerban

<p>Supplementary data file including supplementary figure 1-4 and supplementary table 1-4.</p>

Blocking (statistics)

Infiltration (HVAC)

10.1158/1535-7163.22522093

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Expression profile of miRNA-29a in neural cells

DOAJ (DOAJ: Directory of Open Access Journals) (2015)

Yu Lu Minyu Jian Ye Li Ruquan Han

Objective To investigate the expression profile of microRNA (miRNA)-29a in mice neural cells. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze miRNA-29a expression changes of neurons and astrocytes after 3, 7, 15, 21 d of primary culture in vitro, and cortex tissue of 3, 7, 15, 21 d old mice. Results miRNA-29a expression increased in nervous system with the growth of mice. Compared with the 3th day, miRNA-29a relative expression on the 7th, 15th, 21th days in neurons, astrocytes and cortex tissue were obviously higher ( P < 0.05 or P < 0.01). At each time point, the relative expression levels of miRNA-29a in cultured astrocytes were 20-40 times higher than in cultured neurons ( P = 0.000), and levels in cortex tissue were about 1/3 that seen in cultured astrocytes ( P = 0.000). Conclusions With the growth and development of brain cortex of mice, miRNA-29a is highly expressed in astrocytes, reflecting its abundant and specific expression. DOI: 10.3969/j.issn.1672-6731.2015.01.009

Expression (computer science)

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Neuroprotective effects of microRNA‐211‐5p on chronic stress‐induced neuronal apoptosis and depression‐like behaviours

Journal of Cellular and Molecular Medicine (2021)

Jie Shen Ping Zhang Ye Li Cuiqin Fan Tian Lan

Abstract Findings from recent studies have revealed that microRNAs (miRNAs) are related to numerous neurological disorders. However, whether miRNAs regulate neuronal anomalies involved in the pathogenesis of depression remain unclear. In the present study, we screened miRNA expression profiles in the CA1 hippocampus of a rat model of depression and found that a specific miRNA, microRNA‐211‐5p, was significantly down‐regulated in depressed rats. When miR‐211‐5p was up‐regulated in these rats, neuronal apoptosis within the CA1 area was suppressed, effects which were accompanied with an amelioration of depression‐like behaviours in these rats. These neuroprotective effects of miR‐211‐5p in depressed rats appear to result through suppression of the Dyrk1A/ASK1/JNK signalling pathway within the CA1 area. In further support of this proposal are the findings that knock‐down of miR‐211‐5p within the CA1 area of normal rats activated the Dyrk1A/ASK1/JNK pathway, resulting in the promotion of neuronal apoptosis and display of depression‐like behaviours in these rats. Taken together, these results demonstrate that deficits in miR‐211‐5p contribute to neuronal apoptosis and thus depression‐like behaviours in rats. Therefore, the miR‐211‐5p/Dyrk1A pathway may be critically involved in the pathogenesis of depression and serve as a potential therapeutic target for the treatment of depression.

Depression

Pathogenesis

DYRK1A

10.1111/jcmm.16716

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Citations (18)

Schizophrenia‑associated microRNA‑148b‑3p regulates COMT and PRSS16 expression by targeting the ZNF804A gene in human neuroblastoma cells

Molecular Medicine Reports (2020)

Shanshan Wu Pengjie Wang Ran Tao Pengbo Yang Xiaorui Yu

Zinc finger protein 804A (ZNF804A) has been identified by genome‑wide association studies as a robust risk gene in schizophrenia, but how ZNF804A contributes to schizophrenia and its upstream regulation remains unknown. Previous studies have indicated that microRNAs (miRs) are key factors that regulate the expression levels of their target genes. The present study revealed significantly increased expression of miR‑148b‑3p in the peripheral blood of patients with first‑onset schizophrenia compared with healthy controls, and bioinformatics analysis predicted that the ZNF804A gene is a target of miR‑148b‑3p. Therefore, the present study investigated the possible upstream regulation of ZNF804A by miR‑148b‑3p in the human neuroblastoma SH‑SY5Y cell line, and assessed the implications for schizophrenia. The results revealed significantly reversed expression levels of miR‑148b‑3p (P=0.0051) and ZNF804A (P=0.0218) in the peripheral blood of patients with first‑onset schizophrenia compared with healthy individuals. Furthermore, it was demonstrated that miR‑148b‑3p directly targeted ZNF804A via binding to conserved target sites in the 3'‑untranslated region of ZNF804A mRNA, where it inhibited the endogenous expression of ZNF804A at both the mRNA (P=0.048) and protein levels (P=0.013) in SH‑SY5Y cells. Furthermore, miR‑148b‑3p was revealed to regulate the expression levels of catechol‑O‑methyltransferase (COMT) and serine protease 16 (PRSS16) by targeting ZNF804A in SH‑SY5Y cells. Collectively, the present results indicated that there was a direct upstream regulation of the schizophrenia risk gene ZNF804A by miR‑148b‑3p, which contributed to the regulation of the downstream genes COMT and PRSS16. Thus, the miR‑148b‑3p/ZNF804A/COMT/PRSS16 pathway may play an important role in the pathophysiology of schizophrenia, and may serve as a potential target in drug discovery and gene therapy for this disorder.

10.3892/mmr.2020.11230

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Citations (15)

204P Performance assessment of a comprehensive genomic profiling (CGP) NGS kit across multiple study laboratories

Annals of Oncology (2023)

J. Choi Andrew Fellowes Eli Pikarsky Manuel R. Teixeira I. Vogl

Concordance

10.1016/j.annonc.2023.09.2927

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Citations (1)