A5055667784- Cancer-related Molecular Pathways
- Ubiquitin and proteasome pathways
- Metabolism, Diabetes, and Cancer
- TGF-β signaling in diseases
- Cancer, Hypoxia, and Metabolism
- Pancreatic and Hepatic Oncology Research
- Autophagy in Disease and Therapy
- PI3K/AKT/mTOR signaling in cancer
- Epigenetics and DNA Methylation
- RNA modifications and cancer
- Cancer Research and Treatments
- Hippo pathway signaling and YAP/TAZ
- Dermatology and Skin Diseases
- Exercise and Physiological Responses
- Hedgehog Signaling Pathway Studies
- Pancreatic function and diabetes
- Peptidase Inhibition and Analysis
- IL-33, ST2, and ILC Pathways
- Heat shock proteins research
- Microtubule and mitosis dynamics
- Medical Image Segmentation Techniques
- Hair Growth and Disorders
- Kruppel-like factors research
- Cytokine Signaling Pathways and Interactions
- Mesenchymal stem cell research
Sichuan University
2016-2025
Shanghai Jiao Tong University
2025
Shandong University
2024
State Key Laboratory of Biotherapy
2013-2020
Shaanxi Research Association for Women and Family
2019
Abstract Glucose deprivation, a hallmark of the tumor microenvironment, compels cells to seek alternative energy sources for survival and growth. Here, we show that glucose deprivation upregulates expression mitochondrial-cytochrome c oxidase II (MT-CO2), subunit essential respiratory chain complex IV, in facilitating glutaminolysis sustaining cell survival. Mechanistically, activates Ras signaling enhance MT-CO2 transcription inhibits IGF2BP3, an RNA-binding protein, stabilize mRNA....
The environment of bone marrow mesenchymal stem cells (MSCs) is hypoxic, which plays an important role in maintaining their self-renewal potential and undifferentiated state. MSCs have been proven to possess immunomodulatory properties used clinically treat autoimmune diseases. Here, we tested the effects hypoxia on examined its possible underlying mechanisms. We found that hypoxic stimulation promoted human gingiva–derived (hGMSCs) by enhancing suppressive hGMSCs peripheral blood...
Significance Oncogenic hotspot mutations in PIK3CA and overexpression of HER2 are known as a driving force for human breast cancer metastasis. AMPK is pivotal maintaining cellular energy homeostasis. In this study, we demonstrate that transcription inhibition AMPKα1 critically important advanced with poor clinical outcomes, transcriptionally inhibited response to activation PI3K/HER2, ΔNp63α, tumor metastasis suppressor, direct transcriptional factor mediating oncogenic PI3K/HER2-induced...
Abnormal activation of epidermal growth factor receptor (EGFR) drives non-small cell lung cancer (NSCLC) development. EGFR mutations-mediated resistance to tyrosine-kinase inhibitors (TKIs) is a major hurdle for NSCLC treatment. Here, we show that F-box protein FBXL2 targets and TKI-resistant mutants proteasome-mediated degradation, resulting in suppression EGFR-driven growth. Reduced expression associated with poor clinical outcomes patients. Furthermore, glucose-regulated 94 (Grp94)...
Non-small cell lung cancers (NSCLC) frequently contain KRAS mutation but retain wild-type TP53. Abundant senescent cells are observed in premalignant not malignant tumors derived from the Kras-driven mouse model, suggesting that oncogenic signaling would have to overcome intrinsic senescence burden for cancer progression. Here, we show nuclear Beclin 1-mediated inhibition of p53-dependent drives Kras-mediated tumorigenesis. activates USP5 stabilize 1, leading MDM2-mediated p53 protein...
Reactive oxygen species (ROS) are key regulators in cell proliferation, survival, tumor initiation and development. However, the role of ROS metastasis is less clear. Here, we show that oxidative stress inhibited via activation Hippo kinase MST1/2, which led to phosphorylation nuclear accumulation FoxO3a, resulting upregulation ΔNp63α expression suppression migration independent YAP. Strikingly, while loss MST1 disruption cell-cell junction exemplified by reduced E-cadherin expression,...
Lung cancer stem cells (CSCs) play a pivotal role in tumor development, drug resistance, metastasis and recurrence of lung cancer. Thus, it is great importance to study the mechanism by which CSCs are regulated. In this study, we demonstrate that deubiquitinase USP4 critically important promoting stemness. Silencing leads reduction Oct4 Sox2 expression, decreased CD133+ cell population inhibition tumorsphere formation. Conversely, ectopic expression significantly enhances stemness,...
ABSTRACT The insulin‐like growth factor‐1 (IGF‐1) signaling pathway is known as a potent aging modifier, disruption of which consistently associates with lifespan extension across diverse species. Despite this established association, the mechanisms by IGF‐1 modulates organ remain poorly understood. In study, we assessed age‐related changes in expression multiple organs mice and identified more prominent increase skin levels aging—a phenomenon also observed human skin. To explore...
The influence of the small Rho GTPase Rif (RHOF) on tumor growth, glycolysis, endothelial-mesenchymal transition (EMT), and potential mechanism RHOF in pancreatic cancer (PC) were explored.
Transforming growth factor-β (TGF-β) signaling plays a critical role in promoting epithelial-to-mesenchymal transition (EMT), cell migration, invasion, and tumor metastasis. ΔNp63α, the major isoform of p63 protein expressed epithelial cells, is key transcriptional regulator adhesion program functions as metastasis suppressor. It has been documented that expression ΔNp63α tightly controlled by oncogenic frequently reduced advanced cancers. However, whether TGF-β regulates largely unclear. In...
Tumor metastasis is the major cause of breast cancer morbidity and mortality. It has been reported that F-box protein FBXO3 functions as an E3 ubiquitin ligase in regulating various biological processes, including host autoimmune, antiviral innate immunity, inflammatory response. However, role tumor remains elusive. We have previously shown ΔNp63α a common inhibitory target oncogene-induced cell motility metastasis. In this study, we show plays vital PI3K-mediated independent its activity...
Vincristine is extensively used chemotherapeutic medicine to treat leukemia. However, it remains a critical clinical problem with regard its toxicity and drug-resistance. AMP-activated protein kinase (AMPK) an energy sensor that pivotal in maintaining cell metabolic homeostasis. It reported AMPK involved vincristine-induced apoptosis. whether chemotherapy-resistance largely unclear. well-documented metformin, widely type II diabetes, possesses anti-cancer activities, yet metformin affects...
Accumulating evidence indicates that hotspot p53 mutants have gain-of-function in promoting cell migration and tumor metastasis.However, the molecular mechanisms are not completely understood.Here, we show a mutation, p53-R273H, promotes non-small lung cancer (NSCLC) upregulates mRNA protein expression of neuraminidase-1 (NEU1), sialidase involved proliferation, tumorigenesis.Silencing NEU1 leads to upregulation integrin β4 which significantly inhibits NSCLC induced by...
Tumor growth requires elevated ribosome biogenesis. Targeting ribosomes is an important strategy for cancer therapy. The inhibitor, homoharringtonine (HHT), used the clinical treatment of leukemia, yet it ineffective solid tumors, reasons which remain unclear. Here we show that Snail1, a key factor in regulation epithelial-to-mesenchymal transition, plays pivotal role cellular surveillance response upon ribotoxic stress. Mechanistically, stress activates JNK-USP36 signaling to stabilize...
The Murine Double Minute 2 (MDM2) protein is a key regulator of cell proliferation and apoptosis that acts primarily by inhibiting the p53 tumor suppressor. Similarly, PI3-Kinase (PI3K)/AKT pathway critical for growth factor-mediated survival. Additionally, it has been reported AKT can directly phosphorylate activate MDM2. In this study, we show IGF-1 up-regulates MDM2 levels in PI3K/AKT-dependent manner. Inhibition mTOR rapamycin or expression dominant negative eukaryotic initiation factor...
Abstract Targeted therapy has greatly improved both survival and prognosis of cancer patients. However, while therapeutic treatment adenocarcinoma been advanced greatly, progress in squamous cell carcinoma (SCC) slow ineffective. Therefore, it is great importance to decipher mechanisms identify new drug targets involved development. In this study, we demonstrate that E47 plays the distinctive opposite roles on proliferation carcinoma. While suppresses cells, functions as a oncoprotein...
TGF-β signaling plays a pivotal role in promoting tumor cell migration and cancer metastasis. ΔNp63α TAp63α are two major isoforms of p53-related p63 protein. Our recent study has shown that TGF-β1 promotes protein degradation to facilitate However, whether is involved TGF-β1-induced metastasis remains unclear. In this study, we show that, human pancreatic MIA PaCa-2 cells harboring p53-R248W allele, can significantly inhibit stability Smad pathway-independent manner. Lysosome inhibitor,...
Cell⁻cell adhesion plays an important role in regulation of cell proliferation, migration, survival, and drug sensitivity. Metformin, a first line for type 2 diabetes, has been shown to possess anti-cancer activities. However, whether cell⁻cell affects metformin activity is unknown. In this study, Microscopic FACS analyses showed that induced cancer exemplified by aggregation anoikis under glucose restriction. Furthermore, western blot QPCR revealed dramatically upregulated integrin β1...