A5002065650- Glycosylation and Glycoproteins Research
- Cancer Cells and Metastasis
- Cancer-related Molecular Pathways
- Liver Disease Diagnosis and Treatment
- Epigenetics and DNA Methylation
- Ubiquitin and proteasome pathways
- Galectins and Cancer Biology
- Autophagy in Disease and Therapy
- Lung Cancer Research Studies
- DNA Repair Mechanisms
- Peptidase Inhibition and Analysis
- Dermatologic Treatments and Research
- Protease and Inhibitor Mechanisms
- Genomics and Chromatin Dynamics
- Lung Cancer Treatments and Mutations
- Nerve injury and regeneration
- Calpain Protease Function and Regulation
- Cellular transport and secretion
- Liver physiology and pathology
- Cellular Mechanics and Interactions
- Advanced biosensing and bioanalysis techniques
- Genetic and rare skin diseases.
- Cancer Research and Treatments
- BRCA gene mutations in cancer
- Skin and Cellular Biology Research
Shanghai Jiao Tong University
2009-2025
Zunyi Medical University
2024
Deleted Institution
2011
Dana-Farber Cancer Institute
2006
Harvard University
2006
Boston University
2006
Changsha Medical University
2000-2001
Central South University
1999
There are currently two distinct models proposed to explain why both MDM2 and MDMX required in p53 control, with a key difference centered on whether these inhibitors work together or independently. To test competing models, we generated knockin mice expressing point mutation mutant (C462A) that is defective binding. This approach allowed targeted disassociation of the MDM2/MDMX heterocomplex without affecting ability bind p53, while leaving protein itself completely untouched....
Chemoresistance contributes to cancer relapse and increased mortality in a variety of types, raising pressing need better understand the underlying mechanism. MUC1 is abnormally overexpressed numerous carcinomas associated with poor prognosis. However, functional significance chemoresistance has not been fully elucidated. Here, we showed that expression was considerably induced cells had acquired at both transcriptional post-translational levels. Using gain- loss-of function approaches,...
Abstract Mitophagy is a vital process that controls mitochondria quality, dysregulation of which can promote cancer. Oncoprotein mucin 1 (MUC1) targets to attenuate drug-induced apoptosis. However, little known about whether and how MUC1 contributes mitochondrial homeostasis in cancer cells. We identified novel role promoting mitophagy. Increased mitophagy coupled with the translocation mitochondria, where interacts induces degradation ATPase family AAA domain-containing 3A (ATAD3A),...
Abstract Cancer stem cells (CSCs) are often enriched after chemotherapy and contribute to tumor relapse. While epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) widely used for the treatment of diverse types cancer, whether EGFR-TKIs effective against chemoresistant CSCs in cervical cancer is largely unknown. Here, we reveal that EGFR correlates with reduced disease-free survival patients chemotherapy. Erlotinib, an EGFR-TKI, effectively impedes enrichment...
Telomeres cap the ends of eukaryotic chromosomes and prevent them from being recognized as DNA breaks. We have shown that certain damage responses induced during senescence and, at times telomere uncapping, also can be by treatment cells with small oligonucleotides homologous to 3′ single-strand overhang (T-oligos), implicating this in generation these telomere-based responses. Here, we show T-oligo-treated fibroblasts contain γH2AX foci colocalize telomeres. T-oligos nuclease-resistant are...
Abstract Small cell lung cancer (SCLC) is the most aggressive and lethal subtype of cancer. Cancer stem‐like cells (CSLCs) are primarily responsible for carcinogenesis, therapeutic resistance, tumor recurrence. This study reported that high level mucin1 (MUC1) associated with poor patient survival in SCLC. MUC1 expression peaks during G2/M phase facilitates symmetric division expansion CSLCs. Mechanistically, interaction protein phosphatase 2A (PP2A) results augmented PP2A activity, which...
The ataxia-telangiectasia mutated (ATM) kinase is activated in the cellular response to ionizing radiation (IR) and of importance repair DNA double strand breaks (DSBs). MUC1 oncoprotein aberrantly overexpressed human breast carcinomas. present work demonstrates that C-terminal subunit (MUC1-C) constitutively interacts with ATM cancer cells. We show MUC1-C cytoplasmic domain binds directly HEAT repeats. Our results also demonstrate substrate H2AX. functional significance these interactions...
MUC1 is an oncoprotein that overexpressed in up to 90% of breast carcinomas. A previous vitro study by our group demonstrated the cytoplasmic domain (MUC1-CD), minimal functional unit MUC1, contributes malignant phenotype cells binding directly β-catenin and protecting from GSK3β-induced degradation. To understand vivo role MUC1-CD development, we generated a transgenic mouse model under control MMTV promoter C57BL/6J background, which more resistant tumor. We show expression luminal...
The microenvironment of postpartum mammary gland involution (PMI) has been linked to the increased risk breast cancer and poor outcome patients. Nevertheless mechanism underlying regulates remains largely unknown. MUC1, which is abnormally overexpressed in most cancer, physiologically expressed PMI. Using MUC1 cytoplasm domain (MUC1-CD) transgenic mice, we reveal that overexpression MUC1-CD epithelial cells increases M2 type macrophage infiltration By sustain activating p50, upregulates...
Palladin is an actin cytoskeleton-associated protein which crucial for cell morphogenesis and motility. Previous studies have shown that palladin localized to the axonal growth cone in neurons may play important role extension. Previously, we generated knockout mice display cranial neural tube closure defect embryonic lethality before day 15.5 (E15.5). To further study of developing nervous system, examined innervation palladin-deficient mouse embryos since 200 kd, 140 90-92 kd 50 isoforms...
<title>Abstract</title> Background Biliary atresia (BA) is one of the most common liver diseases in infants and young children. Its etiology pathogenesis are still unclear. The purpose was to investigate mechanism by which highly expressed miRNA-29b exosomes regulates high expression PDGF through methylation, hepatic stellate cell activation, participation fibrosis BA. Methods In previous experiments, peripheral blood children with biliary cholangiectasia (CC) were analyzed, it found that...