A5015555549- Epigenetics and DNA Methylation
- Autophagy in Disease and Therapy
- Cancer, Hypoxia, and Metabolism
- Axon Guidance and Neuronal Signaling
- Angiogenesis and VEGF in Cancer
- Cancer-related gene regulation
- Immune Cell Function and Interaction
- Cell Adhesion Molecules Research
- Immune cells in cancer
- Lymphatic System and Diseases
- Cell death mechanisms and regulation
- Lipid metabolism and biosynthesis
- Endoplasmic Reticulum Stress and Disease
- Melanoma and MAPK Pathways
- Adipokines, Inflammation, and Metabolic Diseases
- Glioma Diagnosis and Treatment
- Cancer, Lipids, and Metabolism
- Apelin-related biomedical research
- Vascular Malformations and Hemangiomas
- Prostate Cancer Treatment and Research
- RNA modifications and cancer
- Liver Disease Diagnosis and Treatment
- Cellular Mechanics and Interactions
- Telomeres, Telomerase, and Senescence
- PARP inhibition in cancer therapy
Sichuan Cancer Hospital
2025
University of Electronic Science and Technology of China
2025
Fuling Center Hospital of Chongqing
2025
Southwest Hospital
2012-2024
Army Medical University
2014-2024
West Cancer Center
2012-2016
National Natural Science Foundation of China
2015
Health First
2015
Fundación Juan March
2015
Christie's
2015
How cancer cells shift metabolism to aerobic glycolysis is largely unknown. Here, we show that deficiency of α/β-hydrolase domain-containing 5 (Abhd5), an intracellular lipolytic activator also known as comparative gene identification 58 (CGI-58), promotes this metabolic and enhances malignancies colorectal carcinomas (CRCs). Silencing Abhd5 in normal fibroblasts induces malignant transformation. Intestine-specific knockout Apc(Min/+) mice robustly increases tumorigenesis transformation...
Overnutrition activates a proinflammatory program in macrophages to induce insulin resistance (IR), but its molecular mechanisms remain incompletely understood. Here, we show that saturated fatty acid and lipopolysaccharide, two factors implicated high-fat diet (HFD)-induced IR, suppress macrophage CGI-58 expression. Macrophage-specific knockout (MaKO) mice aggravates HFD-induced glucose intolerance which is associated with augmented systemic/tissue inflammation activation of adipose tissue...
Abstract Metabolic reprogramming in stromal cells plays an essential role regulating tumour growth. The metabolic activities of tumour-associated macrophages (TAMs) colorectal cancer (CRC) are incompletely characterized. Here, we identify TAM-derived factors and their roles the development CRC. We demonstrate that ABHD5, a lipolytic co-activator, is ectopically expressed CRC-associated macrophages. vitro mouse models macrophage ABHD5 potentiates growth CRC cells. Mechanistically, suppresses...
Triglyceride (TG) accumulation in hepatocytes (hepatic steatosis) preludes the development of advanced nonalcoholic fatty liver diseases (NAFLDs) such as steatohepatitis, fibrosis, and cirrhosis. Mutations human Comparative Gene Identification-58 (CGI-58) cause cytosolic TG-rich lipid droplets to accumulate almost all cell types including hepatocytes. However, it is unclear if CGI-58 mutation causes hepatic steatosis locally or via altering metabolism other tissues. To directly address this...
Cellular senescence is an important tumor-suppressive mechanism. However, acquisition of a senescence-associated secretory phenotype (SASP) in senescent cells has deleterious effects on the tissue microenvironment and, paradoxically, promotes tumor progression. In drug screen, we identified melatonin as novel SASP suppressor human cells. Strikingly, blunts global gene expression upon oncogene-induced (OIS). Moreover, poly(ADP-ribose) polymerase-1 (PARP-1), sensor DNA damage, was new...
Abstract Cancer stemness represents a major source of development and progression colorectal cancer (CRC). c-Met critically contributes to CRC stemness, but how is activated in remains elusive. We previously identified the lipolytic factor ABHD5 as an important tumour suppressor gene CRC. Here, we show that loss promotes activation sustain non-canonical manner. Mechanistically, demonstrate interacts cytoplasm with core subunit SET1A methyltransferase complex, DPY30, thereby inhibiting...
The poor immunogenicity of solid tumors limits the efficacy ofanti-programmed cell death protein 1 (anti-PD1)-based immune checkpoint blockade (ICB); thus, less than 30% patients with cancer exhibit a response. Currently, there is still lack effective strategies for improving tumor immunogenicity.The antitumor effect ultrasound-stimulated nanobubbles (USNBs) alone and in combination an anti-PD1 antibody was evaluated RM1 (prostate cancer), MC38 (colon cancer) B16 (melanoma) xenograft mouse...
Recent evidence has been suggesting the important roles of endothelial cells (ECs) involved in pathogenesis several cancers, including colorectal carcinomas (CRCs), but underlying mechanism remains elusive. We have demonstrated previously that CRC-derived fibronectin extra domain A (EDA) promotes vasculogenesis, tumorigenesis and metastasis CRCs. At current study, we showed EC-secreted EDA metastatic capacity CRC via inducing an epithelial–mesenchymal transition. In vitro vivo experiments...
Autophagy critically contributes to metabolic reprogramming and chromosomal stability. It has been reported that monoallelic loss of the essential autophagy gene BECN1 (encoding BECN1/Beclin 1) promotes cancer development progression. However, mechanism by which is inactivated in malignancy remains largely elusive. We have previously a tumor suppressor role ABHD5 (abhydrolase domain containing 5), co-activator PNPLA2 (patatin like phospholipase 2) colorectal carcinoma (CRC). Here we report...
Objective As the modulation of autophagic processes can be therapeutically beneficial to cancer treatment, identification novel enhancers is highly anticipated. However, current autophagy-inducing anticancer agents exert undesired side effects owing their non-specific biodistribution in off-target tissues. This study aims develop a multifunctional agent integrate targeting, imaging and therapy investigate its mechanism. Design A series mitochondria-targeting near-infrared (NIR) fluorophores...
Abstract The efficacy of Fluorouracil (FU) in the treatment colorectal cancer (CRC) is greatly limited by drug resistance. Autophagy has been implicated chemoresistance, but role selective autophagic degradation regulating chemoresistance remains unknown. In this study, we revealed a critical ABHD5 charging CRC sensitivity to FU via uracil yield. We demonstrated that localizes lysosome and interacts with PDIA5 prevent from interacting RNASET2 inactivating RNASET2. deficiency releases...
The extra domain A (EDA)-containing fibronectin (EDA-FN), an alternatively spliced form of the extracellular matrix protein fibronectin, is predominantly expressed in various malignancies but not normal tissues. In present study, we investigated potential pro-lymphangiogenesis effects (EDA)-mediated vascular endothelial growth factor-C (VEGF-C) secretion colorectal carcinoma (CRC). We detected expressions EDA and VEGF-C 52 human tumor tissues their surrounding mucosae by immunohistochemical...
To elucidate the role of Semaphorin-3F (SEMA3F), originally described as an axon guiding chemorepulsant implicated in nerve development, progression colorectal carcinoma.SEMA3F and its receptor NRP2 were examined 72 cases human carcinoma specimens cell lines LoVo, SW480, SW620 with immunohistochemistry Western blotting. SEMA3F mRNA expression frozen tissue was quantitative reverse transcriptase-PCR. Confocal laser scanning microscopy used for detection cellular localization proteins by...
Tumor cells acquire the capacity of resistance to chemotherapy or radiotherapy via cell-matrix and cell-cell crosstalk. Integrins are most important cell adhesion molecules, in which αV integrin mainly mediating tight contact between tumor cells.
Abstract The fusion genes NRG1 and NRG2, members of the epidermal growth factor (EGF) receptor family, have emerged as key drivers in cancer. Upon fusion, retains its EGF-like active domain, binds to ERBB ligand triggers intracellular signaling cascades, promoting uncontrolled cell proliferation. incidence gene varies across cancer types, with lung being most prevalent at 0.19 0.27%. CD74 SLC3A2 are frequently observed partners. RNA-based next-generation sequencing is primary method for...
The constrained cross-talk between myeloid cells and T in the tumor immune microenvironment (TIME) restricts cancer immunotherapy efficacy, whereas underlying mechanism remains elusive. Parkin, an E3 ubiquitin ligase renowned for mitochondrial quality control, has emerged as a regulator of response. Here, we show that both systemic macrophage-specific ablations Parkin mice lead to attenuated progression prolonged mouse survival. By single-cell RNA-seq flow cytometry, demonstrate deficiency...
Endostatin is a natural occurring anti-angiogenic peptide and has been shown to inhibit tumor lymphangiogenesis by suppressing the expression of tumor-stimulating growth factors. We have previously that fibronectin alternative extra domain A (EDA) facilitates colorectal tumors. Since it known EDA interacts with integrin α9 in lymphatic endothelial cells (LECs), we hypothesized endostatin may target EDA-integrin pathway tumor-induced lymphangiogenesis. To test this hypothesis, examined effect...
Controversies have arisen from recent mouse studies about the essential role of biliary sterol secretion in reverse cholesterol transport (RCT). The objective this study was to examine modulating macrophage RCT Niemann-Pick C1-Like 1 (NPC1L1) liver only (L1(LivOnly)) mice, an animal model that is defective both and intestinal absorption, determine whether NPC1L1 inhibitor ezetimibe facilitates by inhibiting hepatic NPC1L1.L1(LivOnly) mice were generated crossing knockout (L1-KO) with...