Tien Luyen Vu

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phctlv@nus.edu.sg


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PHARMACOLOGY
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2021 - 20234
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Now showing 1 - 4 of 4
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    alpha v beta 1 integrin is enriched in extracellular vesicles of metastatic breast cancer cells: A mechanism mediated by galectin-3
    (WILEY, 2022-08-01) Zhang, Daniel Xin; Dang, Xuan TT; Vu, Luyen Tien; Lim, Claudine Ming Hui; Yeo, Eric Yew Meng; Lam, Brenda Wan Shing; Leong, Sai Mun; Omar, Noorjehan; Putti, Thomas Choudary; Yeh, Yu Chen; Ma, Victor; Luo, Jia-Yuan; Cho, William C; Chen, Gang; Lee, Victor Kwan Min; Grimson, Andrew; Le, Minh TN; Assoc Prof Thomas Choudary Putti; PHARMACOLOGY; PAEDIATRICS; PATHOLOGY
    Breast cancer cells release a large quantity of biocargo-bearing extracellular vesicles (EVs), which mediate intercellular communication within the tumour microenvironment and promote metastasis. To identify EV-bound proteins related to metastasis, we used mass spectrometry to profile EVs from highly and poorly metastatic breast cancer lines of human and mouse origins. Comparative mass spectrometry indicated that integrins, including αv and β1 subunits, are preferentially enriched in EVs of highly metastatic origin over those of poorly metastatic origin. These results are consistent with our histopathological findings, which show that integrin αv is associated with disease progression in breast cancer patients. Integrin αv colocalizes with the multivesicular-body marker CD63 at a higher frequency in the tumour and is enriched in circulating EVs of breast cancer patients at late stages when compared with circulating EVs from early-stage patients. With a magnetic bead-based flow cytometry assay, we confirmed that integrins αv and β1 are enriched in the CD63+ subsets of EVs from both human and mouse highly metastatic cells. By analysing the level of integrin αv on circulating EVs, this assay could predict the metastatic potential of a xenografted mouse model. To explore the export mechanism of integrins into EVs, we performed immunoprecipitation mass spectrometry and identified members of the galectin family as potential shuttlers of integrin αvβ1 into EVs. In particular, knockdown of galectin-3, but not galectin-1, causes a reduction in the levels of cell surface integrins β1 and αv, and decreases the colocalization of these integrins with CD63. Importantly, knockdown of galectin-3 leads to a decrease of integrin αvβ1 export into the EVs concomitant with a decrease in the metastatic potential of breast cancer cells. Moreover, inhibition of the integrin αvβ1 complex leads to a reduction in the binding of EVs to fibronectin, suggesting that integrin αvβ1 is important for EV retention in the extracellular matrix. EVs retained in the extracellular matrix are taken up by fibroblasts, which differentiate into cancer associated fibroblasts. In summary, our data indicate an important link between EV-bound integrin αvβ1 with breast cancer metastasis and provide additional insights into the export of integrin αvβ1 into EVs in the context of metastasis.
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    Red Blood Cell-Derived Extracellular Vesicles Display Endogenous Antiviral Effects and Enhance the Efficacy of Antiviral Oligonucleotide Therapy
    (AMER CHEMICAL SOC, 2023-10-18) Jayasinghe, Migara K; Gao, Chang; Yap, Gracemary; Yeo, Brendon Zhi Jie; Vu, Luyen Tien; Tay, Douglas Jie Wen; Loh, Wen Xiu; Aw, Zhen Qin; Chen, Huixin; Phung, Dai Cao; Hoang, Dong Van; Prajogo, Rebecca Carissa; Hooi, Lissa; Lim, Fang Qing; Pirisinu, Marco; Mok, Chee Keng; Lim, Kah Wai; Tang, Sze Jing; Tan, Kai Sen; Chow, Edward Kai-Hua; Chen, Leilei; Phan, Anh Tuan; Chu, Justin Jang Hann; Le, Minh TN; Dr Yan Ling Ng; PHARMACOLOGY; DEAN'S OFFICE (MEDICINE); SURGERY; ANATOMY; MICROBIOLOGY AND IMMUNOLOGY; CANCER SCIENCE INSTITUTE OF SINGAPORE
    The COVID-19 pandemic has resulted in a large number of fatalities and, at present, lacks a readily available curative treatment for patients. Here, we demonstrate that unmodified red blood cell-derived extracellular vesicles (RBCEVs) can inhibit SARS-CoV-2 infection in a phosphatidylserine (PS) dependent manner. Using T cell immunoglobulin mucin domain-1 (TIM-1) as an example, we demonstrate that PS receptors on cells can significantly increase the adsorption and infection of authentic and pseudotyped SARS-CoV-2 viruses. RBCEVs competitively inhibit this interaction and block TIM-1-mediated viral entry into cells. We further extend the therapeutic efficacy of this antiviral treatment by loading antisense oligonucleotides (ASOs) designed to target conserved regions of key SARS-CoV-2 genes into RBCEVs. We establish that ASO-loaded RBCEVs are efficiently taken up by cells in vitro and in vivo to suppress SARS-CoV-2 replication. Our findings indicate that this RBCEV-based SARS-CoV-2 therapeutic displays promise as a potential treatment capable of inhibiting SARS-CoV-2 entry and replication.
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    Surface-engineered extracellular vesicles for targeted delivery of therapeutic RNAs and peptides for cancer therapy
    (Ivyspring International Publisher, 2022) Jayasinghe, Migara Kavishka; Pirisinu, Marco; Yang, Yuqi; Peng, Boya; Pham, Thach Tuan; Lee, Chang Yu; Tan, Melissa; Vu, Luyen Tien; Dang, Xuan TT; Pham, Tin Chanh; Chen, Huan; Leung, Anskar YH; Cho, William C; Shi, Jiahai; Le, Minh TN; Dr Le Thi Nguyet Minh; PHARMACOLOGY; CHEMICAL & BIOMOLECULAR ENGINEERING
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    MicroRNA-29 specifies age-related differences in the CD8+ T cell immune response
    (Elsevier B.V., 2021-11-01) Yee Mon, Kristel J.; Zhu, Hongya; Daly, Ciaran W. P.; Vu, Luyen T.; Smith, Norah L.; Patel, Ravi; Topham, David J.; Scheible, Kristin; Jambo, Kondwani; Le, Minh T. N.; Rudd, Brian D.; Grimson, Andrew; PHARMACOLOGY
    MicroRNAs (miRNAs) have emerged as critical regulators of cell fate in the CD8+ T cell response to infection. Although there are several examples of miRNAs acting on effector CD8+ T cells after infection, it is unclear whether differential expression of one or more miRNAs in the naive state is consequential in altering their long-term trajectory. To answer this question, we examine the role of miR-29 in neonatal and adult CD8+ T cells, which express different amounts of miR-29 only prior to infection and adopt profoundly different fates after immune challenge. We find that manipulation of miR-29 expression in the naive state is sufficient for age-adjusting the phenotype and function of CD8+ T cells, including their regulatory landscapes and long-term differentiation trajectories after infection. Thus, miR-29 acts as a developmental switch by controlling the balance between a rapid effector response in neonates and the generation of long-lived memory in adults. © 2021 The Authors