A5077316829- Cancer Immunotherapy and Biomarkers
- Cancer, Hypoxia, and Metabolism
- Osteoarthritis Treatment and Mechanisms
- Hippo pathway signaling and YAP/TAZ
- Cancer-related molecular mechanisms research
- Glioma Diagnosis and Treatment
- Cancer-related gene regulation
- Pancreatic and Hepatic Oncology Research
- Cancer Genomics and Diagnostics
- CAR-T cell therapy research
- Prostate Cancer Treatment and Research
- Epigenetics and DNA Methylation
- PI3K/AKT/mTOR signaling in cancer
- Ferroptosis and cancer prognosis
- Cytokine Signaling Pathways and Interactions
- Immunotherapy and Immune Responses
- Cancer Cells and Metastasis
- Immune cells in cancer
- Inhalation and Respiratory Drug Delivery
- Spine and Intervertebral Disc Pathology
- Melanoma and MAPK Pathways
- MicroRNA in disease regulation
- RNA modifications and cancer
- Ubiquitin and proteasome pathways
- Cancer, Lipids, and Metabolism
Chongqing Medical University
2025
Chinese Academy of Agricultural Sciences
2023-2024
Agricultural Genomics Institute at Shenzhen
2023-2024
Shanghai Chest Hospital
2023-2024
Shanghai Jiao Tong University
2023-2024
Scripps MD Anderson Cancer Center
2024
Memorial Sloan Kettering Cancer Center
2013-2024
Psychogenics (United States)
2015-2023
The University of Texas MD Anderson Cancer Center
2014-2023
Kettering University
2016-2023
Immune checkpoint blockade represents a major breakthrough in cancer therapy; however, responses are not universal. Genomic and immune features pretreatment tumor biopsies have been reported to correlate with response patients melanoma other cancers, but robust biomarkers identified. We studied cohort of metastatic initially treated cytotoxic T-lymphocyte-associated antigen-4 (CTLA4) (n = 53) followed by programmed death-1 (PD-1) at progression 46), analyzed signatures longitudinal tissue...
Immune checkpoint blockade produces clinical benefit in many patients. However, better biomarkers of response are still needed, and mechanisms resistance remain incompletely understood. To address this, we recently studied a cohort melanoma patients treated with sequential against cytotoxic T lymphocyte antigen-4 (CTLA-4) followed by programmed death receptor-1 (PD-1) identified immune markers resistance. Building on these studies, performed deep molecular profiling including cell receptor...
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,...
We have investigated the importance of interleukin-6 (IL-6) in promoting tumor growth and metastasis. In human primary breast cancers, increased levels IL-6 were found at leading edge positively correlated with advanced stage, suggesting a mechanistic link between cell production invasion. support this hypothesis, we showed that IL-6/Janus kinase (JAK)/signal transducer activator transcription 3 (Stat3) pathway drives progression through stroma metastatic niche. Overexpression lines promoted...
Resistance to neoadjuvant chemotherapy in triple-negative breast cancer can be mediated by a reversible chemotherapy-tolerant state.
Abstract A hallmark of pancreatic ductal adenocarcinoma (PDAC) is an exuberant stroma comprised diverse cell types that enable or suppress tumor progression. Here, we explored the role oncogenic KRAS in protumorigenic signaling interactions between cancer cells and host cells. We show mutation (KRAS*) drives cell-autonomous expression type I cytokine receptor complexes (IL2rγ–IL4rα IL2rγ–IL13rα1) turn are capable receiving growth signals (IL4 IL13) provided by invading Th2 microenvironment....
Cyclin-dependent kinases 4 and 6 (CDK4/6) represent a major therapeutic vulnerability for breast cancer. The are clinically targeted via ATP competitive inhibitors (CDK4/6i); however, drug resistance commonly emerges over time. To understand CDK4/6i resistance, we surveyed 1,300 cancers identified several genetic alterations (e.g., FAT1, PTEN, or ARID1A loss) converging on upregulation of CDK6. Mechanistically, demonstrate CDK6 causes by inducing binding CDK inhibitor INK4 proteins...
PCOS is a common metabolic disorder in women of reproductive age, which pathogenesis very complex. The role ferroptosis novel finding, and the mechanistic studies are not clear. Metformin commonly used drug but few on whether metformin can improve follicle development ovarian function PCOS. We aims to use mouse model study effect based explored regulation mice by intervening pathway.C57 BL/6J female aged 4-5 weeks were purchased gavaged with letrozole (1 mg/kg/day) combined high-fat diet for...
Abstract The mechanisms of metastatic progression from hormonal therapy (HT) are largely unknown in luminal breast cancer. Here we demonstrate the enrichment CD133 hi /ER lo cancer cells clinical specimens following neoadjuvant endocrine and HT refractory disease. We develop experimental models that can promote generation HT-resistant, self-renewing /IL6 stem (CSCs). initially abrogates oxidative phosphorylation (OXPHOS) generating self-renewal-deficient cells, /OXPHOS . These exit metabolic...
The hypothesis that microvesicle-mediated miRNA transfer converts noncancer stem cells into cancer (CSC) leading to therapy resistance remains poorly investigated. Here we provide direct evidence supporting this hypothesis, by demonstrating how microvesicles derived from cancer-associated fibroblasts (CAF) miR-221 promote hormonal (HTR) in models of luminal breast cancer. We determined CAF-derived horizontally transferred tumor and, combination with hormone therapy, activated an ER
Though the efficacy of MEK inhibitors is being investigated in KRAS-mutant colorectal cancers (CRC), early clinical trials inhibitor monotherapy did not reveal significant antitumor activity. Resistance to developed through a variety mechanisms converging ERK reactivation. Since increases cyclin D expression and entry into cell cycle, we hypothesized that combination CDK4/6 would have synergistic activity cause tumor regression vivo.The synergistically inhibited cancer growth vitro caused...
Abstract Genetic inactivation of PTEN is common in prostate cancer and correlates with poorer prognosis. We previously identified CHD1 as an essential gene PTEN-deficient cells. Here, we sought definitive vivo genetic evidence for, mechanistic understanding of, the role cancer. In Pten Pten/Smad4 genetically engineered mouse models, prostate-specific deletion Chd1 resulted markedly delayed tumor progression prolonged survival. was associated profound microenvironment (TME) remodeling...
Molecular imaging probes have potential for in vivo identification of apoptosis and other intracellular processes. TcapQ, a cell-penetrating, near-infrared fluorescent peptide probe designed to be optically silent through intramolecular fluorescence quenching activated by effector caspases, has been previously described validated vitro. Herein, using NMDA-induced retinal ganglion cells (RGCs), representing an rat model glaucoma, we assessed the ability TcapQ image single-cell caspase...
Apoptosis is required for normal cellular homeostasis, and deregulation of the apoptotic process implicated in various diseases. Previously, we developed a cell-penetrating near-infrared fluorescence (NIRF) probe based on an activatable strategy to detect apoptosis-associated caspase activity vivo. This consisted Tat peptide conjugated effector recognition sequence (DEVD) that was flanked by fluorophore−quencher pair (Alexa Fluor 647 QSY 21). Once exposed caspases, cleaved, resulting...
A key feature of high-grade serous ovarian carcinoma (HGSOC) is frequent amplification the 3q26 locus harboring PRKC-ι ( PRKCI ). Here, we show that also expressed in early fallopian tube lesions, called tubal intraepithelial carcinoma. Transgenic mouse studies establish as an cancer-specific oncogene. Mechanistically, oncogenic activity relates part to up-regulation TNFα promote immune-suppressive tumor microenvironment characterized by abundance myeloid-derived suppressor cells and...
Intervertebral disc degeneration (IDD) is associated with dysregulated expression of microRNAs (miRNAs). However, the precise molecular mechanisms underlying this disorder remain unclear. Therefore, we tested hypothesis that miRNAs modulate IDD through effects on IL-6/STAT3 signaling pathway, a potential regulator IDD. The miRNA profile was determined in nucleus pulposus (NP) tissues from patients and controls, employing microarray quantitative real-time PCR (RT-qPCR). Biological functions...