A5019378272- Hippo pathway signaling and YAP/TAZ
- Pancreatic and Hepatic Oncology Research
- Cancer, Hypoxia, and Metabolism
- Cancer Genomics and Diagnostics
- Phagocytosis and Immune Regulation
- Epigenetics and DNA Methylation
- Cancer, Lipids, and Metabolism
- Cancer Research and Treatments
- Metabolism, Diabetes, and Cancer
- Ubiquitin and proteasome pathways
- Cancer-related gene regulation
- RNA modifications and cancer
- Cellular Mechanics and Interactions
- Protease and Inhibitor Mechanisms
- Cell Adhesion Molecules Research
- Caveolin-1 and cellular processes
- Cancer-related Molecular Pathways
- Ferroptosis and cancer prognosis
- CRISPR and Genetic Engineering
- Prostate Cancer Treatment and Research
- Cancer Cells and Metastasis
- Cancer Immunotherapy and Biomarkers
- Proteoglycans and glycosaminoglycans research
- Single-cell and spatial transcriptomics
- Endoplasmic Reticulum Stress and Disease
The University of Texas MD Anderson Cancer Center
2015-2025
The University of Texas Health Science Center at Houston
2024
Scripps MD Anderson Cancer Center
2024
Fudan University Shanghai Cancer Center
2011-2014
Shanghai Medical College of Fudan University
2008-2013
Fudan University
2012-2013
Ministry of Education of the People's Republic of China
2010
East China University of Science and Technology
2009
Abstract The signaling mechanisms between prostate cancer cells and infiltrating immune may illuminate novel therapeutic approaches. Here, utilizing a adenocarcinoma model driven by loss of Pten Smad4, we identify polymorphonuclear myeloid-derived suppressor (MDSC) as the major cell type, depletion MDSCs blocks progression. Employing dual reporter model, epithelial stromal transcriptomic profiling identified CXCL5 cancer-secreted chemokine to attract CXCR2-expressing MDSCs, and,...
Inflammation is a major risk factor for pancreatic ductal adenocarcinoma (PDAC). When occurring in the context of pancreatitis, KRAS mutations accelerate tumor development mouse models. We report that long after its complete resolution, transient inflammatory event primes epithelial cells to subsequent transformation by oncogenic KRAS. Upon recovery from acute inflammation, display an enduring adaptive response associated with sustained transcriptional and epigenetic reprogramming. Such...
Despite substantial advances in targeting mutant KRAS, tumor resistance to KRAS inhibitors (KRASi) remains a major barrier progress. Here, we report proteostasis reprogramming as key convergence point of multiple KRASi-resistance mechanisms. Inactivation oncogenic down-regulated both the heat shock response and inositol-requiring enzyme 1α (IRE1α) branch unfolded protein response, causing severe disturbances. However, IRE1α was selectively reactivated an ER stress–independent manner acquired...
A number of oncoproteins and tumor suppressors are known to be neddylated, but whether the neddylation pathway is entirely activated in human cancer remains unexplored.NEDD8-activating enzyme (NAE) (E1) NEDD8-conjugating (E2) expression global-protein were examined by immunohistochemistry, immunoblotting, real-time polymerase chain reaction analysis. Cell proliferation, clonogenic survival, migration, motility vitro, as well formation metastasis vivo, determined upon inhibition MLN4924, an...
Current treatment regimens for pancreatic ductal adenocarcinoma (PDAC) yield poor 5-year survival, emphasizing the critical need to identify druggable targets essential PDAC maintenance. We developed an unbiased and in vivo target discovery approach molecular vulnerabilities low-passage patient-derived xenografts or genetically engineered mouse model-derived allografts. Focusing on epigenetic regulators, we identified WDR5, a core member of COMPASS histone H3 Lys4 (H3K4) MLL (1-4)...
Integrin αvβ3 receptor is expressed on several types of cancer cells, including pancreatic and plays an important role in tumor growth metastasis. The ability to target the integrin cells increases efficacy targeted therapy reduces side effects. aim this study develop a novel arginine-glycine-aspartic acid (RGD) peptide-conjugated albumin nanoparticle enhance intracellular uptake anticancer drug into through receptor-mediated endocytosis. In cellular studies, fluorescent signal...
Abstract Mutated KRAS (KRAS*) is a fundamental driver in the majority of pancreatic ductal adenocarcinomas (PDAC). Using an inducible mouse model KRAS*-driven PDAC, we compared KRAS* genetic extinction with pharmacologic inhibition MEK1 tumor spheres and vivo. ablation blocked proliferation induced apoptosis, whereas exerted cytostatic effects. Proteomic analysis evidenced that was accompanied by sustained activation PI3K–AKT–MTOR pathway AXL, PDGFRa, HER1–2 receptor tyrosine kinases (RTK)...
Transcriptomic profiling classifies pancreatic ductal adenocarcinoma (PDAC) into several molecular subtypes with distinctive histological and clinical characteristics. However, little is known about the mechanisms that define each subtype their correlation outcome. Mutant KRAS most prominent driver in PDAC, present over 90% of tumors, but dependence tumors on oncogenic signaling varies between subtypes. In particular, squamous relatively independent typically displays much more aggressive...
Abstract Mitochondria are hubs where bioenergetics, redox homeostasis, and anabolic metabolism pathways integrate through a tightly coordinated flux of metabolites. The contributions mitochondrial to tumor growth therapy resistance evident, but drugs targeting have repeatedly failed in the clinic. Our study pancreatic ductal adenocarcinoma (PDAC) finds that cellular lipid composition influence cancer cell sensitivity pharmacological inhibition electron transport chain complex I. Profiling...
Tumor cells exhibit abnormal actin remodeling profiles, which involve the altered expressions of several important actin-binding proteins. Profilin1 (Pfn1), originally identified as an actin-associated protein, has been linked to human malignancies. Our recent studies suggested that Pfn1 facilitates apoptosis in pancreatic cancer cells. Here, we investigated exact role (Pfn1) adenocarcinoma (PDAC) and underlying mechanisms. protein expression PDAC specimens was analyzed by...
Abstract Capitalizing on the inherent multiplexing capability of AsCpf1, we developed a multiplexed, high-throughput screening strategy that minimizes library size without sacrificing gene targeting efficiency. We demonstrated AsCpf1 can be used for functional genomics screenings and an AsCpf1-based multiplexed performs similarly as compared to currently available monocistronic CRISPR/Cas9 libraries, with only one vector required each gene. construct smallest whole-genome CRISPR knock-out...
Deregulated expression of zinc transporters was linked to several cancers. However, the detailed profile all human in normal organs and cancer, especially pancreatic cancer is not available. The objectives this study are investigate complete patterns 14 ZIP 10 ZnT a large number tissues cell lines. We examined 22 different tissues, 11 pairs clinical specimens surrounding normal/benign as well established lines plus ductal epithelium (HPDE) cells, using real time RT-PCR immunohistochemistry....
Methyl-CpG binding domain protein 1 (MBD1) has been implicated in transcriptional regulation, heterochromatin formation, genomic stability, cell-cycle progression and development. It is also predicted that MBD1 might be involved tumor development progression. However, whether how tumorigenesis, especially pancreatic cancer (PC), currently unknown. We found was significantly up-regulated PC tissues compared with the surrounding normal according to RT-PCR data. Tissue microarray (TMA) based...
Abstract Pancreatic ductal adenocarcinoma (PDAC) is almost universally lethal. A critical unmet need exists to explore essential susceptibilities in PDAC and identify druggable targets improve treatment. KRAS mutations dominate the genetic landscape of lead activation multiple downstream pathways cellular processes. Here, we investigated requirement these for tumor maintenance using an inducible KrasG12D-driven mouse model (iKras model), identifying that RAF-MEK-MAPK signaling major effector...
Abstract Entosis, a form of cell-in-cell (CIC) structure formation where one cell invades and becomes internalized by another, has long been observed in various malignancies is considered critical cellular process cancer progression, with potential impacts on tumor heterogeneity, survival, metastasis. Syndecan-1 (SDC1), transmembrane proteoglycan involved adhesion communication, plays pivotal role these processes, yet its specific function entosis within pancreatic ductal adenocarcinoma...