Query：
学者姓名：卢钟磊
Refining：
Year
Type
Indexed by
Source
Complex
Former Name
Co-
Language
Clean All
Abstract ：
The development of RNA interference (RNAi) therapy offers a potential solution for Alzheimer's disease (AD). However, the brain-blood barrier (BBB) with its selective permeability and pharmacokinetic-related challenges poses restrictions on the delivery of small interfering RNA (siRNA) to the central nervous system (CNS). In this study, we demonstrate that the incorporation of 2 '-fluoro (2 '-F) substitutions and L-carnitine modification facilitates the self-assembly of siRNA through triple interaction, leading to the formation of nanorings, called LCSF-NR. Based on the enhanced cellular uptake and lysosomal escape by 2 '-F substitution and the transport across the BBB promoted by L-carnitine, the nanorings realized the improved brain-targeted delivery of siRNA, both in zebrafish and mice models. Moreover, our findings highlight the therapeutic potential of LCSF-NR formulation in an AD zebrafish model through a synergistic effect of downregulating the beta-site APP cleavage enzyme 1 (BACE1) gene and L-carnitine-mediated neuroprotection, effectively inhibiting pathological processes. Overall, these results suggest that the chemical modification-based siRNA self-assembly strategy enables trans-BBB delivery and presents a concise approach for synergistic therapy of AD.
Keyword ：
Alzheimer's disease Alzheimer's disease blood-brain barrier blood-brain barrier chemical modification chemical modification self-assembly self-assembly siRNA siRNA
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Jiang, Yifan , Li, Lisha , Fang, Xiao et al. Self-assembling chemically modified siRNA nanorings for RNAi therapy and neuroprotection in Alzheimer's disease [J]. | SCIENCE CHINA-CHEMISTRY , 2025 . |
| MLA | Jiang, Yifan et al. "Self-assembling chemically modified siRNA nanorings for RNAi therapy and neuroprotection in Alzheimer's disease" . | SCIENCE CHINA-CHEMISTRY (2025) . |
| APA | Jiang, Yifan , Li, Lisha , Fang, Xiao , Zeng, Tao , Su, Lichao , Liu, Yichang et al. Self-assembling chemically modified siRNA nanorings for RNAi therapy and neuroprotection in Alzheimer's disease . | SCIENCE CHINA-CHEMISTRY , 2025 . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
Soft-tissue sarcomas (STS) emerges as formidable challenges in clinics due to the complex genetic heterogeneity, high rates of local recurrence and metastasis. Exploring specific targets and biomarkers would benefit the prognosis and treatment of STS. Here, we identified RCC1, a guanine-nucleotide exchange factor for Ran, as an oncogene and a potential intervention target in STS. Bioinformatics analysis indicated that RCC1 is highly expressed and correlated with poor prognosis in STS. Functional studies showed that RCC1 knockdown significantly inhibited the cell cycle transition, proliferation and migration of STS cells in vitro, and the growth of STS xenografts in mice. Mechanistically, we identified Skp2 as a downstream target of RCC1 in STS. Loss of RCC1 substantially diminished Skp2 abundance by compromising its protein stability, resulting in the upregulation of p27Kip1 and G1/S transition arrest. Specifically, RCC1 might facilitate the nucleo-cytoplasmic trafficking of Skp2 via direct interaction. As a result, the cytoplasmic retention of Skp2 would further protect it from ubiquitination and degradation. Notably, recovery of Skp2 expression largely reversed the phenotypes induced by RCC1 knockdown in STS cells. Collectively, this study unveils a novel RCC1-Skp2-p27Kip1 axis in STS oncogenesis, which holds promise for improving prognosis and treatment of this formidable malignancy.
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Zhuang, Mingzhi , Li, Fengyue , Liang, Hong et al. Targeting RCC1 to block the human soft-tissue sarcoma by disrupting nucleo-cytoplasmic trafficking of Skp2 [J]. | CELL DEATH & DISEASE , 2024 , 15 (4) . |
| MLA | Zhuang, Mingzhi et al. "Targeting RCC1 to block the human soft-tissue sarcoma by disrupting nucleo-cytoplasmic trafficking of Skp2" . | CELL DEATH & DISEASE 15 . 4 (2024) . |
| APA | Zhuang, Mingzhi , Li, Fengyue , Liang, Hong , Su, Yongfu , Cheng, Lei , Lin, Bingkai et al. Targeting RCC1 to block the human soft-tissue sarcoma by disrupting nucleo-cytoplasmic trafficking of Skp2 . | CELL DEATH & DISEASE , 2024 , 15 (4) . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
The relevant mechanism of tumor-associated macrophages (TAMs) in the treatment of colorectal cancer patients with immune checkpoint inhibitors (ICIs) is discussed, and the application prospects of TAMs in reversing the treatment tolerance of ICIs are discussed to provide a reference for related studies. As a class of drugs widely used in clinical tumor immunotherapy, ICIs can act on regulatory molecules on cells that play an inhibitory role - immune checkpoints - and kill tumors in the form of an immune response by activating a variety of immune cells in the immune system. The sensitivity of patients with different types of colorectal cancer to ICI treatment varies greatly. The phenotype and function of TAMs in the colorectal cancer microenvironment are closely related to the efficacy of ICIs. ICIs can regulate the phenotypic function of TAMs, and TAMs can also affect the tolerance of colorectal cancer to ICI therapy. TAMs play an important role in ICI resistance, and making full use of this target as a therapeutic strategy is expected to improve the immunotherapy efficacy and prognosis of patients with colorectal cancer.
Keyword ：
Colorectal cancer Colorectal cancer Colorectal cancer stem cells Colorectal cancer stem cells Review Review Tumor immune microenvironment Tumor immune microenvironment Tumor metastasis Tumor metastasis
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Deng, Run-Zhi , Zheng, Xin , Lu, Zhong-Lei et al. Effect of colorectal cancer stem cells on the development and metastasis of colorectal cancer [J]. | WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY , 2024 , 16 (11) . |
| MLA | Deng, Run-Zhi et al. "Effect of colorectal cancer stem cells on the development and metastasis of colorectal cancer" . | WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY 16 . 11 (2024) . |
| APA | Deng, Run-Zhi , Zheng, Xin , Lu, Zhong-Lei , Yuan, Ming , Meng, Qi-Chang , Wu, Tao et al. Effect of colorectal cancer stem cells on the development and metastasis of colorectal cancer . | WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY , 2024 , 16 (11) . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
Hepatocellular carcinoma (HCC) poses a significant threat due to its highly aggressive and high recurrence characteristics, necessitating urgent advances in diagnostic and therapeutic approaches. Long non-coding RNAs exert vital roles in HCC tumorigenesis, however the mechanisms of their expression regulation and functions are not fully elucidated yet. Herein, we identify that a novel tumor suppressor 'lnc-PIK3R1' was significantly downregulated in HCC tissues, which was correlated with poor prognosis. Functionally, lnc-PIK3R1 played tumor suppressor roles to inhibit the proliferation and mobility of HCC cells, and to impede the distant implantation of xenograft in mice. Mechanistic studies revealed that lnc-PIK3R1 interacted with miR-1286 and alleviated the repression on GSK3B by miR-1286. Notably, pharmacological inhibition of GSK3 beta compromised the tumor suppression effect by lnc-PIK3R1, confirming their functional relevance. Moreover, we identified that oncogenic YY1 acts as a specific transcriptional repressor to downregulate the expression of lnc-PIK3R1 in HCC. In summary, this study highlights the tumor-suppressive effect of lnc-PIK3R1, and provides new insights into the regulation of GSK3 beta expression in HCC, which would benefit the development of innovative intervention strategies for HCC.
Keyword ：
GSK3 beta GSK3 beta Hepatocellular carcinoma (HCC) Hepatocellular carcinoma (HCC) miR-1286 miR-1286
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Lyu, Peng , Li, Fengyue , Deng, Runzhi et al. Lnc-PIK3R1, transcriptionally suppressed by YY1, inhibits hepatocellular carcinoma progression via the Lnc-PIK3R1/miR-1286/GSK3β axis [J]. | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE , 2024 , 1870 (6) . |
| MLA | Lyu, Peng et al. "Lnc-PIK3R1, transcriptionally suppressed by YY1, inhibits hepatocellular carcinoma progression via the Lnc-PIK3R1/miR-1286/GSK3β axis" . | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE 1870 . 6 (2024) . |
| APA | Lyu, Peng , Li, Fengyue , Deng, Runzhi , Wei, Qiliang , Lin, Bingkai , Cheng, Lei et al. Lnc-PIK3R1, transcriptionally suppressed by YY1, inhibits hepatocellular carcinoma progression via the Lnc-PIK3R1/miR-1286/GSK3β axis . | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE , 2024 , 1870 (6) . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
Objective: We retrospectively studied cancer mortality and incidence in China from 1990 to 2019, investigated the cancer trends and risk factors, and analyzed the effects of Gross Domestic Product (GDP) on cancer mortality and incidence. Methods: Data was obtained in "Our world in data" in October 2022 to explore mortality rates of different cancers and their trends and the roles of cancer risk factors, including GDP, air pollution, etc. Results: Over the past 30 years, cancer had been China's second leading cause of death. Tracheal, bronchial, and lung cancers, with an annual growth rate of 6.5%, were the most frequently diagnosed cancers. The burden of different cancers changed as the mortality rate of cancer changed. The age-standardized cancer mortality rate had decreased by 19.0%; cancer deaths in all age groups had increased. While the number of cancer deaths in the elderly aged & GE;70 did not increase distinctively, its percentage increased by 52.1% and 1.7% annually. The percentage of patients with new-onset cancer increased by 240% and 8.6% annually. For every USD 1,000 increase in GDP, cancer deaths decreased by 2.3/100,000. Tobacco, meat, and alcohol consumption and BMI had increased and were not conducive to the future control of cancer. Conclusions: We summarized the incidence and mortality of major cancers and their trends in China over the past 30 years and analyzed the effects of GDP and the roles of cancer risk factors. Overall GDP growth and effective control of air pollution reduced cancer mortality, while population aging, smoking, alcohol consumption, BMI increasing, and meat consumption brought challenges for cancer control.
Keyword ：
cancer control cancer control cancer mortality cancer mortality Cancer trends Cancer trends China China GDP GDP risk factor risk factor
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Wu, Weiwei , Zhang, Ruochen , Jin, Yiming et al. Cancer trends and risk factors in China over the past 30 years (1990-2019) [J]. | JOURNAL OF CANCER , 2023 , 14 (10) : 1935-1945 . |
| MLA | Wu, Weiwei et al. "Cancer trends and risk factors in China over the past 30 years (1990-2019)" . | JOURNAL OF CANCER 14 . 10 (2023) : 1935-1945 . |
| APA | Wu, Weiwei , Zhang, Ruochen , Jin, Yiming , Lu, Yan , Lu, Zhonglei , Li, Tao et al. Cancer trends and risk factors in China over the past 30 years (1990-2019) . | JOURNAL OF CANCER , 2023 , 14 (10) , 1935-1945 . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
Background Tumor cells can resist chemotherapy-induced pyroptosis through glycolytic reprogramming. Estrogen-related receptor alpha (ERR alpha) is a central regulator of cellular energy metabolism associated with poor cancer prognosis. Herein, we refine the oncogenic role of ERR alpha in the pyroptosis pathway and glycolytic metabolism.Methods The interaction between ERR alpha and HIF-1 alpha was verified using co-immunoprecipitation. The transcriptional binding sites of ERR alpha and NLRP3 were confirmed using dual-luciferase reporter assay and cleavage under targets and tagmentation (CUT&Tag). Flow cytometry, transmission electron microscopy, scanning electron microscopy, cell mito stress test, and extracellular acidification rate analysis were performed to investigate the effects of ERR alpha on the pyroptosis pathway and glycolytic metabolism. The results of these experiments were further confirmed in endometrial cancer (EC)-derived organoids and nude mice. In addition, the expression of ERR alpha-related pyroptosis genes was analyzed using The Cancer Genome Atlas and Gene Expression Omnibus database.Results Triggered by a hypoxic microenvironment, highly expressed ERR alpha could bind to the promoter of NLRP3 and inhibit caspase-1/GSDMD signaling, which reduced inflammasome activation and increased pyroptosis resistance, thereby resulting in the resistance of cancer cells to cisplatin. Moreover, ERR alpha activated glycolytic rate-limiting enzyme to bridge glycolytic metabolism and pyroptosis in EC. This phenomenon was further confirmed in EC-derived organoids and nude mice. CUT & Tag sequencing and The Cancer Genome Atlas database analysis showed that ERR alpha participated in glycolysis and programmed cell death, which resulted in EC progression.Conclusions ERR alpha inhibits pyroptosis in an NLRP3-dependent manner and induces glycolytic metabolism, resulting in cisplatin resistance in EC cells.
Keyword ：
Cisplatin resistance Cisplatin resistance Endometrial cancer Endometrial cancer ERR alpha ERR alpha Metabolic reprogramming Metabolic reprogramming Pyroptosis Pyroptosis
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Su, Pingping , Mao, Xiaodan , Ma, Jincheng et al. ERRα promotes glycolytic metabolism and targets the NLRP3/caspase-1/GSDMD pathway to regulate pyroptosis in endometrial cancer [J]. | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH , 2023 , 42 (1) . |
| MLA | Su, Pingping et al. "ERRα promotes glycolytic metabolism and targets the NLRP3/caspase-1/GSDMD pathway to regulate pyroptosis in endometrial cancer" . | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 42 . 1 (2023) . |
| APA | Su, Pingping , Mao, Xiaodan , Ma, Jincheng , Huang, Lixiang , Yu, Lirui , Tang, Shuting et al. ERRα promotes glycolytic metabolism and targets the NLRP3/caspase-1/GSDMD pathway to regulate pyroptosis in endometrial cancer . | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH , 2023 , 42 (1) . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
Advanced prostate cancer, harboring multiple mutations of tumor suppressor genes, is refractory to conventional therapies. Knockout of the Skp2 gene blocks pRb/p53 doubly deficient prostate cancer in mice, which inspired the authors to develop an approach for delivering siRNA that would efficiently silence Skp2 (siSkp2) in vivo. Here, a facile strategy is reported to directly assemble siSkp2 with the natural compound quercetin (Que) into supramolecular nanoparticles (NPs). This carrier-free siSkp2 delivery system could effectively protect siSkp2 from degradation in serum and enhance its cellular internalization. Furthermore, the siSkp2/Que NPs exhibit synergistic effects in Skp2 silencing, because they can degrade the mRNA and protein of Skp2 simultaneously. Indeed, siSkp2/Que NPs remarkably diminish the Skp2 abundance and further inhibit the proliferation and migration of TMU cells (RB1/TP53/KRAS triple mutations) in vitro. The in vivo results further show that i.v. administration of siSkp2/Que NPs efficiently accumulates in tumor sites and strongly inhibits the growth of TMU tumors in nude mice. Importantly, the siSkp2/Que NPs do not induce any abnormality in the treated mice, which suggests satisfactory biocompatibility. Collectively, this study describes a tractable siRNA self-assembled strategy for Skp2 silencing, which might be a promising nanodrug to cure multitherapy-resistant advanced prostate cancer.
Keyword ：
advanced prostate cancer advanced prostate cancer nanodrugs nanodrugs self-assembly self-assembly siRNA delivery siRNA delivery Skp2 Skp2
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Liang, Hong , Zhang, Fangming , Hong, Yannv et al. Synergistic Silencing of Skp2 by siRNA Self-Assembled Nanoparticles as a Therapeutic Strategy for Advanced Prostate Cancer [J]. | SMALL , 2022 , 18 (14) . |
| MLA | Liang, Hong et al. "Synergistic Silencing of Skp2 by siRNA Self-Assembled Nanoparticles as a Therapeutic Strategy for Advanced Prostate Cancer" . | SMALL 18 . 14 (2022) . |
| APA | Liang, Hong , Zhang, Fangming , Hong, Yannv , Wu, Yue , Xie, Huanzhang , Zhang, Chen et al. Synergistic Silencing of Skp2 by siRNA Self-Assembled Nanoparticles as a Therapeutic Strategy for Advanced Prostate Cancer . | SMALL , 2022 , 18 (14) . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
Loss of neuron homeostasis in the arcuate nucleus (ARC) is responsible for diet-induced-obesity (DIO). We previously reported that loss of Rb1 gene compromised the homeostasis of anorexigenic POMC neurons in ARC and induced obesity in mice. To evaluate the development of DIO, we propose to analyze the transcriptomic alteration of POMC neurons in mice following high fat diet (HFD) feeding. We isolated these neurons from established DIO mice and performed transcriptomic profiling using RNA-seq. In total, 1066 genes (628 upregulated and 438 downregulated) were identified as differentially expressed genes (DEGs). Pathway enrichment analysis with these DEGs further revealed that "cell cycle," "apoptosis," "chemokine signaling," and "sphingo-lipid metabolism" pathways were correlated with DIO development. Moreover, we validated that the pRb protein, a key regulator of "cell cycle pathway," was inactivated by phosphorylation in POMC neurons by HFD feeding. Importantly, the reversal of deregulated cell cycle by stereotaxic delivering of the unphosphorylated pRb.P in ARC significantly meliorated the DIO. Collectively, our study provides insights into the mechanisms related to the loss of homeostasis of POMC neurons in DIO, and suggests pRb phosphorylation as a potential intervention target to treat DIO.
Keyword ：
Diet-induced obesity (DIO) Diet-induced obesity (DIO) High-fat-diet (HFD) High-fat-diet (HFD) Neuron homeostasis Neuron homeostasis POMC neuron POMC neuron pRb phosphorylation pRb phosphorylation
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Lyu, Peng , Huang, Zhishun , Feng, Qingjun et al. Unveiling the transcriptome alteration of POMC neuron in diet-induced obesity [J]. | EXPERIMENTAL CELL RESEARCH , 2020 , 389 (1) . |
| MLA | Lyu, Peng et al. "Unveiling the transcriptome alteration of POMC neuron in diet-induced obesity" . | EXPERIMENTAL CELL RESEARCH 389 . 1 (2020) . |
| APA | Lyu, Peng , Huang, Zhishun , Feng, Qingjun , Su, Yongfu , Zheng, Mengying , Hong, Yannv et al. Unveiling the transcriptome alteration of POMC neuron in diet-induced obesity . | EXPERIMENTAL CELL RESEARCH , 2020 , 389 (1) . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
近年来,因肥胖症所造成的社会问题和医疗负担越发严重.肥胖主要是由于机体能量的摄入与消耗不平衡所致,而中枢神经系统以及相关神经元在机体能量代谢平衡的调控中发挥着重要作用.下丘脑弓状核含有抑食性阿黑皮素原(Proopiomelanocortin,POMC)神经元和促食性神经肽Y(Neuropeptid Y,NPY)/刺鼠相关蛋白(Agouti-related protein,AgRP)神经元,是调控机体摄食行为的主要神经元.研究显示,高脂饮食会诱导POMC神经元中的Rb蛋白发生磷酸化修饰并失活,导致POMC神经元从静息状态重新进入细胞周期循环,进而迅速转向细胞凋亡.高脂饮食也会引起神经元再生抑制,并诱导炎症发生和神经元损伤,使神经元稳态失衡,引发瘦素抵抗,最终导致肥胖症的发生.文中就神经元稳态失衡以及肥胖症等疾病之间的关系进行了综述,希望能为饮食诱导肥胖症等疾病的治疗和预防提供新的方向和思路.
Keyword ：
神经元稳态失衡 神经元稳态失衡 肥胖症 肥胖症 高脂饮食 高脂饮食
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | 黄智舜 , 郑梦盈 , 冯庆君 et al. 神经元稳态失衡和饮食诱导肥胖症的相关性研究进展 [J]. | 生物工程学报 , 2019 , 35 (8) : 1433-1440 . |
| MLA | 黄智舜 et al. "神经元稳态失衡和饮食诱导肥胖症的相关性研究进展" . | 生物工程学报 35 . 8 (2019) : 1433-1440 . |
| APA | 黄智舜 , 郑梦盈 , 冯庆君 , 洪燕女 , 卢钟磊 . 神经元稳态失衡和饮食诱导肥胖症的相关性研究进展 . | 生物工程学报 , 2019 , 35 (8) , 1433-1440 . |
| Export to | NoteExpress RIS BibTex |
Version ：
Abstract ：
When obesity is caused by consumption of a high-fat diet, the tumor suppressor pRb is phosphoinactivated in the neurons of the mediobasal hypothalamus, a brain area critical for energy-balance regulation. However, the functional relevance of pRb phosphoinactivation in the mediobasal hypothalamus to diet-induced obesity remains unknown. Here, we show that inhibiting pRb phosphorylation in the mediobasal hypothalamus can prevent and treat diet-induced obesity in mice. Expressing an unphosphorylable pRb nonselectively in the mediobasal hypothalamus or conditionally in anorexigenic POMC neurons inhibits diet-induced obesity. Intracerebroventricular delivery of US Food and Drug Administration-approved (FDA-approved) cyclin-dependent kinase 4 (CDK4) inhibitor abemaciclib inhibits pRb phosphorylation in the mediobasal hypothalamus and prevents diet-induced obesity. Oral administration of abemaciclib at doses approved for human use reduces fat mass in diet-induced obese mice by increasing lipid oxidation without significantly reducing lean mass. With analysis of recent literature identifying CDK4 as the most abundantly expressed neuronal CDK in the mediobasal hypothalamus, our work uncovers CDK4 as the major kinase for hypothalamic pRb phosphoinactivation and a highly effective central antiobesity target. As three CDK4/6 inhibitors have recently received FDA approval for life-long breast cancer therapy, our study provides a preclinical basis for their expedient repurposing for obesity management.
Cite：
Copy from the list or Export to your reference management。
| GB/T 7714 | Iqbal, Niloy Jafar , Lu, Zhonglei , Liu, Shun Mei et al. Cyclin-dependent kinase 4 is a preclinical target for diet-induced obesity [J]. | JCI INSIGHT , 2018 , 3 (17) . |
| MLA | Iqbal, Niloy Jafar et al. "Cyclin-dependent kinase 4 is a preclinical target for diet-induced obesity" . | JCI INSIGHT 3 . 17 (2018) . |
| APA | Iqbal, Niloy Jafar , Lu, Zhonglei , Liu, Shun Mei , Schwartz, Gary J. , Chua, Streamson, Jr. , Zhu, Liang . Cyclin-dependent kinase 4 is a preclinical target for diet-induced obesity . | JCI INSIGHT , 2018 , 3 (17) . |
| Export to | NoteExpress RIS BibTex |
Version ：
Export
| Results： |
Selected to |
| Format： |
