Yunlong Yang

ORCID: 0000-0003-1551-9828
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About
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Research Areas
  • Angiogenesis and VEGF in Cancer
  • Cancer, Hypoxia, and Metabolism
  • Fibroblast Growth Factor Research
  • Adipose Tissue and Metabolism
  • Adipokines, Inflammation, and Metabolic Diseases
  • Cancer Cells and Metastasis
  • Lymphatic System and Diseases
  • IL-33, ST2, and ILC Pathways
  • Cardiovascular Disease and Adiposity
  • Neurobiology and Insect Physiology Research
  • Kruppel-like factors research
  • Cancer Immunotherapy and Biomarkers
  • Erythropoietin and Anemia Treatment
  • Microbial Natural Products and Biosynthesis
  • Cancer, Stress, Anesthesia, and Immune Response
  • Endoplasmic Reticulum Stress and Disease
  • Animal Disease Management and Epidemiology
  • Hippo pathway signaling and YAP/TAZ
  • Nanoplatforms for cancer theranostics
  • Immune Cell Function and Interaction
  • Zebrafish Biomedical Research Applications
  • Vector-Borne Animal Diseases
  • Phagocytosis and Immune Regulation
  • Diet and metabolism studies
  • Hepatocellular Carcinoma Treatment and Prognosis

Sichuan University
2024-2025

Fudan University
2012-2025

South China Agricultural University
2021-2025

Guangzhou Experimental Station
2025

Karolinska Institutet
2011-2022

Shenzhen Second People's Hospital
2016-2022

Suzhou Municipal Hospital
2021

Texas A&M University
2013-2019

Texas A&M University System
2019

Shriners Hospitals for Children - Boston
2017-2018

Significance We show that vascular pericytes significantly contribute to cancer invasion and metastasis by the mechanism of pericyte–fibroblast transition (PFT). This study proposes this concept indicates pericyte’s role. Vascular were considered remodel tumor vessels toward a mature phenotype. However, once dissociated from their functions within tissue are not known. In present study, we pericytes, detached microvasculatures, underwent differentiation become stromal fibroblasts, which...

10.1073/pnas.1608384113 article EN Proceedings of the National Academy of Sciences 2016-09-07

Glucose uptake is essential for cancer glycolysis and involved in non-shivering thermogenesis of adipose tissues1-6. Most cancers use to harness energy their infinite growth, invasion metastasis2,7,8. Activation thermogenic metabolism brown tissue (BAT) by cold drugs instigates blood glucose adipocytes4,5,9. However, the functional effects global metabolic changes associated with BAT activation on tumour growth are unclear. Here we show that exposure tumour-bearing mice conditions markedly...

10.1038/s41586-022-05030-3 article EN cc-by Nature 2022-08-03

Significance PD-L1 is well known as an immune checkpoint molecule, which suppresses surveillance through binding to its receptor PD-1. Intracellular can also protect messenger RNAs of several DNA damage repair–related genes from degradation and enhance tumor resistance DNA-damaging therapy. Triple-negative breast cancer (TNBC) has the worst prognosis highest risk distant relapse in shows immunotherapy radiotherapy. In this study, we found that D-mannose promote significantly radiotherapy...

10.1073/pnas.2114851119 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2022-02-18

Pancreatic ductal adenocarcinoma (PDAC) is the most lethal malignancy and lacks effective treatment. We aimed to understand molecular mechanisms of intertwined interactions between tumour stromal components in metastasis provide a new paradigm for PDAC therapy.

10.1136/gutjnl-2020-322744 article EN Gut 2021-02-10

Signalling molecules and pathways that mediate crosstalk between various tumour cellular compartments in cancer metastasis remain largely unknown. We report a mechanism of the interaction perivascular cells tumour-associated macrophages (TAMs) promoting through IL-33-ST2-dependent pathway xenograft mouse models cancer. IL-33 is highest upregulated gene activation SOX7 transcription factor PDGF-BB-stimulated pericytes. Gain- loss-of-function experiments validate promotes recruitment TAMs....

10.1038/ncomms11385 article EN cc-by Nature Communications 2016-05-06

Significance Cancer metastasis is responsible for a majority of the mortality in cancer patients and involves complex interactions, modulated by various factors cytokines, between malignant host cells. Vascular structures solid tumors are crucial cell intravasation into circulation. Our present work shows that VEGF-B produced tumor cells significantly remodels microvasculature, leading to leaky vascular networks highly permissive invasion. VEGF-B–promoted occurs through VEGF-A–independent...

10.1073/pnas.1503500112 article EN Proceedings of the National Academy of Sciences 2015-05-19

Systemic therapy with anti-VEGF drugs such as bevacizumab is widely used for treatment of human patients various solid tumors. However, systemic impacts in host healthy vasculatures remain poorly understood. Here, we show that, mice, delivery an or anti–VEGF receptor (VEGFR)-2 neutralizing antibody caused global vascular regression. Among all examined tissues, endocrine glands, intestinal villi, and uterus are the most affected response to VEGF VEGFR-2 blockades. Thyroid fenestrations were...

10.1073/pnas.1301331110 article EN Proceedings of the National Academy of Sciences 2013-07-01

Molecular mechanisms underlying the cancer stroma in metastasis need further exploration. Here, we discovered that cancer-associated fibroblasts (CAFs) produced high levels of IL-33 acted on tumor-associated macrophages (TAMs), causing them to undergo M1 M2 transition. Genomic profiling metastasis-related genes IL-33-stimulated TAMs showed a >200-fold increase MMP9. Signaling analysis demonstrated IL-33-ST2-NF-κB-MMP9-laminin pathway governed tumor stroma-mediated metastasis. In mouse and...

10.1172/jci.insight.122375 article EN JCI Insight 2018-10-17

Abstract The impact of discontinuation anti-VEGF cancer therapy in promoting metastasis is unknown. Here we show treatment creates a time-window profound structural changes liver sinusoidal vasculatures, exhibiting hyper-permeability and enlarged open-pore sizes the fenestrated endothelium loss VE-cadherin. drug cessation caused highly leaky hepatic vasculatures permit tumour cell intravasation extravasation. Discontinuation an antibody-based sunitinib markedly promotes metastasis....

10.1038/ncomms12680 article EN cc-by Nature Communications 2016-09-01

Abstract Cold- and β3-adrenoceptor agonist-induced sympathetic activation leads to angiogenesis UCP1-dependent thermogenesis in mouse brown white adipose tissues. Here we show that endothelial production of PDGF-CC during tissue (WAT) regulates WAT browning. We find genetic deletion VEGFR2, knockout the Pdgf-c gene or pharmacological blockade PDGFR-α impair WAT-beige transition. further stimulation upregulates UCP1 expression acquisition a beige phenotype differentiated WAT-PDGFR-α +...

10.1038/ncomms12152 article EN cc-by Nature Communications 2016-08-05

Abstract FGF-2 displays multifarious functions in regulation of angiogenesis and vascular remodeling. However, effective drugs for treating + tumors are unavailable. Here we show that modulates tumor vessels by recruiting NG2 pricytes onto microvessels through a PDGFRβ-dependent mechanism. intrinsically resistant to clinically available targeting VEGF PDGF. Surprisingly, dual the PDGF signaling produces superior antitumor effect breast cancer fibrosarcoma models. Mechanistically, inhibition...

10.1038/s41467-020-17525-6 article EN cc-by Nature Communications 2020-07-24

Molecular signaling in the tumor microenvironment (TME) is complex, and crosstalk among various cell compartments supporting metastasis remains poorly understood. In particular, role of vascular pericytes, a critical cellular component TME, cancer invasion warrants further investigation. Here, we report that an elevation FGF-2 samples from patients with nasopharyngeal carcinoma (NPC) xenograft mouse models promoted NPC metastasis. Mechanistically, cell-derived strongly pericyte proliferation...

10.1172/jci.insight.157874 article EN cc-by JCI Insight 2022-04-19

Vessel co-option has been demonstrated to mediate colorectal cancer liver metastasis (CRCLM) resistance antiangiogenic therapy. The current mechanisms underlying vessel have mainly focused on "hijacker" tumor cells, whereas the function of "hijackee" sinusoidal blood vessels not explored. Here, we found that occurrence in bevacizumab-resistant CRCLM xenografts was associated with increased expression fibroblast activation protein α (FAPα) co-opted hepatic stellate cells (HSCs), which...

10.1172/jci157399 article EN cc-by Journal of Clinical Investigation 2022-08-11

Although VEGF-B was discovered as a VEGF-A homolog long time ago, the angiogenic effect of remains poorly understood with limited and diverse findings from different groups. Notwithstanding, drugs that inhibit together other VEGF family members are being used to treat patients various neovascular diseases. It is therefore critical have better understanding underlying mechanisms. Using comprehensive in vitro vivo methods models, we reveal here for first an unexpected surprising function...

10.1038/s41392-023-01539-9 article EN cc-by Signal Transduction and Targeted Therapy 2023-08-18

Immune checkpoint blockade (ICB) has revolutionized the treatment of various cancer types. Despite significant preclinical advancements in understanding mechanisms, identifying molecular basis and predictive biomarkers for clinical ICB responses remains challenging. Recent evidence, both clinical, underscores pivotal role extracellular matrix (ECM) modulating immune cell infiltration behaviors. This study aimed to create an innovative classifier that leverages ECM characteristics enhance...

10.1002/cac2.12538 article EN cc-by-nc-nd Cancer Communications 2024-03-20

Molecular mechanisms underlying circadian-regulated physiological processes remain largely unknown. Here, we show that disruption of the circadian clock by both constant exposure to light and genetic manipulation key genes in zebrafish led impaired developmental angiogenesis. A bmal1-specific morpholino inhibited angiogenesis embryos without causing obvious nonvascular phenotypes. Conversely, a period2 accelerated angiogenic vessel growth, suggesting Bmal1 Period2 display opposing effects....

10.1016/j.celrep.2012.07.005 article EN cc-by-nc-nd Cell Reports 2012-08-01

Purpose: Cancer metastasis can occur at the early stage of tumor development when a primary is microscopic size. In particular, interaction malignant cells with other cell types including cancer-associated fibroblasts (CAF) in promoting remains largely unknown. Here, we investigated role CAFs facilitating initial events cancer tumors were sizes.Experimental Design: Multicolor-coded and coimplanted into transparent zebrafish body single-cell level was monitored living animals. Healthy...

10.1158/1078-0432.ccr-17-0101 article EN Clinical Cancer Research 2017-04-19

Significance Mirabegron as a β3-adrenoceptor agonist is routinely prescribed drug for treating overactive bladder syndrome. However, the effect of this on off-targeted tissues and organs largely unknown. In study, we provide mechanistic insights mirabegron-triggered atherosclerosis in causing potential cardiovascular cerebrovascular diseases by activation brown fat. Given that mirabegron can induce fat adult human subjects, these findings are clinically relevant. Moreover, genetic mutations...

10.1073/pnas.1901655116 article EN Proceedings of the National Academy of Sciences 2019-05-13
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