Prof. Tang-Long Shen
Professor
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Academic Career Length
27Years (2000-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications28 October 2015 in Nature
Journal Article
AHAyuko Hoshino
Ayuko Hoshino
BCBruno Costa-Silva
Bruno Costa-SilvaTang-Long ShenGRGoncalo Rodrigues
Goncalo Rodrigues
AHAyako Hashimoto
Ayako Hashimoto
DLDavid Lyden
David Lyden +48
Ever since Stephen Paget’s 1889 hypothesis, metastatic organotropism has remained one of cancer’s greatest mysteries. Here we demonstrate that exosomes from mouse and human lung-, liver- and brain-tropic tumour cells fuse preferentially with resident cells at their predicted destination, namely lung fibroblasts and epithelial cells, liver Kupffer cells and brain endothelial cells. We show that tumour-derived exosomes uptaken by organ-specific cells prepare the pre-metastatic niche. Treatment with exosomes from lung-tropic models redirected the metastasis of bone-tropic tumour cells. Exosome proteomics revealed distinct integrin expression patterns, in which the exosomal integrins α6β4 and α6β1 were associated with lung metastasis, while exosomal integrin αvβ5 was linked to liver metastasis. Targeting the integrins α6β4 and αvβ5 decreased exosome uptake, as well as lung and liver metastasis, respectively. We demonstrate that exosome integrin uptake by resident cells activates Src phosphorylation and pro-inflammatory S100 gene expression. Finally, our clinical data indicate that exosomal integrins could be used to predict organ-specific metastasis.
18 May 2015 in Nature Cell Biology
Journal Article
BCBruno Costa-Silva
Bruno Costa-SilvaNANicole M. Aiello
Nicole M. AielloAOAllyson J. Ocean
Allyson J. Ocean
SSSwarnima Singh
Swarnima Singh
HZHaiying Zhang
Haiying Zhang
DLDavid Lyden
David Lyden +31
16 June 2018 in Cancer Science
Journal Article
YTYu-Ling TAi
Yu-Ling TAiKCKo‐Chien Chen
Ko‐Chien ChenJHJer‐Tsong Hsieh
Jer‐Tsong Hsieh
Tang-Long ShenExosomes participate in cancer progression and metastasis by transferring bioactive molecules between cancer and various cells in the local and distant microenvironments. Such intercellular cross‐talk results in changes in multiple cellular and biological functions in recipient cells. Several hallmarks of cancer have reportedly been impacted by this exosome‐mediated cell‐to‐cell communication, including modulating immune responses, reprogramming stromal cells, remodeling the architecture of the extracellular matrix, or even endowing cancer cells with characteristics of drug resistance. Selectively, loading specific oncogenic molecules into exosomes highlights exosomes as potential diagnostic biomarkers as well as therapeutic targets. In addition, exosome‐based drug delivery strategies in preclinical and clinical trials have been shown to dramatically decrease cancer development. In the present review, we summarize the significant aspects of exosomes in cancer development that can provide novel strategies for potential clinical applications.
20 June 2005 in Journal of Cell Biology
Journal Article
Tang-Long ShenAPAnn Y.-J. Park
Ann Y.-J. Park
AAAna Alcaraz
Ana Alcaraz
XPXu Peng
Xu Peng
IJIhnkyung Jang
Ihnkyung Jang
JGJun-Lin Guan
Jun-Lin Guan +3
Focal adhesion kinase (FAK) is a critical mediator of signal transduction by integrins and growth factor receptors in a variety of cells including endothelial cells (ECs). Here, we describe EC-specific knockout of FAK using a Cre-loxP approach. In contrast to the total FAK knockout, deletion of FAK specifically in ECs did not affect early embryonic development including normal vasculogenesis. However, in late embryogenesis, FAK deletion in the ECs led to defective angiogenesis in the embryos, yolk sac, and placenta, impaired vasculature and associated hemorrhage, edema, and developmental delay, and late embryonic lethal phenotype. Histologically, ECs and blood vessels in the mutant embryos present a disorganized, detached, and apoptotic appearance. Consistent with these phenotypes, deletion of FAK in ECs isolated from the floxed FAK mice led to reduced tubulogenesis, cell survival, proliferation, and migration in vitro. Together, these results strongly suggest a role of FAK in angiogenesis and vascular development due to its essential function in the regulation of multiple EC activities.
17 October 2004 in Nature Neuroscience
Journal Article
WLWeiquan Li
Weiquan Li
JLJeeyong Lee
Jeeyong Lee
HVHaris G Vikis
Haris G Vikis
SLSeung-Hee Lee
Seung-Hee Lee
GLGuofa Liu
Guofa Liu
KGKun-Liang Guan
Kun-Liang Guan +7
1 January 2015 in BioMed Research International
Journal Article
Focal adhesion kinase (FAK) is a cytoplasmic nonreceptor tyrosine kinase that enables activation by growth factor receptors or integrins in various types of human cancers. The kinase-dependent and kinase-independent scaffolding functions of FAK modulate the authentic signaling and fundamental functions not only in cancer cells but also in tumor microenvironment to facilitate cancer progression and metastasis. The overexpression and activation of FAK are usually investigated in primary or metastatic cancers and correlated with the poor clinical outcome, highlighting FAK as a potential prognostic marker and anticancer target. Small molecule inhibitors targeting FAK kinase activity or FAK-scaffolding functions impair cancer development in preclinical or clinical trials. In this review, we give an overview for FAK signaling in cancer cells as well as tumor microenvironment that provides new strategies for the invention of cancer development and malignancy.
About Me
Prof. Tang-Long Shen received his BS and MS degrees from National Taiwan University in the Department of Plant Pathology, and obtained his PhD from Cornell University in the Department of Molecular Medicine. After his postdoc training in American Heart Association, Prof. Shen has joined the Department of Plant Pathology and Microbiology at the National Taiwan University. His research explores varied subjects, including microbes, plants to human, to understand the basic mechanisms of various pathologic complications as well as how to utilize the microbial metabolites or natural product for human health. By using molecular biology, biochemistry and cellular biology approaches as well as animal models, Prof. Shen deciphers the molecular mechanism of cancer progression, especially how cancer cells interact with tumor microenvironment in cell migration, the formation of pre-metastatic niches and metastatic organotropism. Several key targets, including integrins, receptor tyrosine kinases (e.g. EGFR), non-receptor tyrosine kinases (e.g. FAK, Src), adaptor proteins (e.g. Grb7, C35) and cytokines as well as extracellular vesicles (e.g. exosomes), are main focuses. Additionally, Shen lab is also seeking useful natural products and de novo protein components in human cells including critical secondary metabolites from traditional Chinese medicinal fungi, Cordyceps spp, Antrodia cinnamomea, and metallothioneins, to apply for anti-cancer,