A5055155526- TGF-β signaling in diseases
- Ubiquitin and proteasome pathways
- Cancer-related gene regulation
- MicroRNA in disease regulation
- RNA modifications and cancer
- Hippo pathway signaling and YAP/TAZ
- Pancreatic and Hepatic Oncology Research
- Genetic factors in colorectal cancer
- Kruppel-like factors research
- interferon and immune responses
- Metabolism, Diabetes, and Cancer
- PI3K/AKT/mTOR signaling in cancer
- Cancer Cells and Metastasis
- Cancer, Hypoxia, and Metabolism
- Cell Adhesion Molecules Research
- NF-κB Signaling Pathways
- Lung Cancer Treatments and Mutations
- Renal and related cancers
- HER2/EGFR in Cancer Research
- Peptidase Inhibition and Analysis
- Cerebrovascular and genetic disorders
- RNA Research and Splicing
- Protein Tyrosine Phosphatases
- Cancer-related Molecular Pathways
- RNA Interference and Gene Delivery
Zhejiang University
2016-2025
Shaoxing University
2022-2025
Center for Life Sciences
2022-2025
Zhejiang International Studies University
2025
Zhejiang Cancer Hospital
2021-2024
Second Affiliated Hospital of Zhejiang University
2017-2024
Hangzhou Cancer Hospital
2024
Baylor College of Medicine
2013-2023
Huazhong Agricultural University
2019-2023
Institute of Life Sciences
2023
N6-methyladenosine (m6A) is enriched in 3'untranslated region (3'UTR) and near stop codon of mature polyadenylated mRNAs mammalian systems has regulatory roles eukaryotic mRNA transcriptome switch. Significantly, the mechanism for this modification preference remains unknown, however. Herein we report a characterization full m6A methyltransferase complex HeLa cells identifying METTL3/METTL14/WTAP/VIRMA/HAKAI/ZC3H13 as key components, show that VIRMA mediates preferential methylation 3'UTR...
Smads regulate transcription of defined genes in response to TGF-β receptor activation, although the mechanisms Smad-mediated are not well understood. We demonstrate that TGF-β-inducible Smad3 uses tumor suppressor Smad4/DPC4 and CBP/p300 as transcriptional coactivators, which associate with TGF-β. The association CBP was localized carboxyl terminus Smad3, is required for a segment CBP. Furthermore, stimulated both TGF-β- Smad-induced Smad4/DPC4-dependent fashion. transactivation...
Smads are important intracellular signaling effectors for transforming growth factor-β (TGF-β) and related factors. Proper TGF-β requires precise control of Smad functions. In this study, we have identified a novel HECT class ubiquitin E3 ligase, designated Smurf2, that negatively regulates Smad2 signaling. both yeast two-hybrid in vitro binding assays, found Smurf2 could interact with receptor-activated (R-Smads), including Smad1, Smad2, Smad3 but not Smad4. Ectopic expression was...
Objective Hepatocellular carcinoma (HCC) is heterogeneous, especially in multifocal tumours, which decreases the efficacy of clinical treatments. Understanding tumour heterogeneity critical when developing novel treatment strategies. However, a comprehensive investigation HCC lacking, and available evidence regarding has not led to improvements practice. Design We harvested 42 samples from eight patients evaluated using whole-exome sequencing, RNA mass spectrometry-based proteomics...
Tumor infiltrated type II (M2) macrophages promote tumorigenesis by suppressing immune clearance, promoting proliferation, and stimulating angiogenesis. Interestingly, were also found to enrich in small foci of altered hepatocytes containing liver tumor-initiating cells (TICs). However, whether how TICs specifically recruit the function these tumor initiation remain unknown due technical difficulties. In this study, generating genetically defined TICs, we demonstrate that actively M2 from as...
The unfolded protein response (UPR) is a cellular homeostatic mechanism that activated in many human cancers and plays pivotal roles tumor progression therapy resistance. However, the molecular mechanisms for UPR activation regulation cancer cells remain elusive. Here, we show oncogenic MYC regulates inositol-requiring enzyme 1 (IRE1)/X-box binding (XBP1) branch of breast via multiple mechanisms. We found directly controls IRE1 transcription by to its promoter enhancer. Furthermore, forms...
Cytosolic double-stranded DNA surveillance by cyclic GMP-AMP synthase (cGAS)-Stimulator of Interferon Genes (STING) signaling triggers cellular senescence, autophagy, biased mRNA translation, and interferon-mediated immune responses. However, detailed mechanisms physiological relevance STING-induced senescence are not fully understood. Here, we unexpectedly found that interferon regulatory factor 3 (IRF3), activated during innate sensing, forms substantial endogenous complexes in the nucleus...
Caspase-3 is a critical enzyme for apoptosis and cell survival. Here we report delayed ossification decreased bone mineral density in caspase-3–deficient (Casp3–/– Casp3+/–) mice due to an attenuated osteogenic differentiation of marrow stromal stem cells (BMSSCs). The mechanism involved the impaired BMSSCs due, at least partially, overactivated TGF-β/Smad2 signaling pathway upregulated expressions p53 p21 along with downregulated Cdk2 Cdc2, ultimately increased replicative senescence. In...
Smad7 plays an essential role in the negative-feedback regulation of transforming growth factor beta (TGF-beta) signaling by inhibiting TGF-beta at receptor level. It can interfere with binding to type I receptors and thus activation receptor-regulated Smads or recruit E3 ubiquitin ligase Smurf target them for degradation. Here, we report that is predominantly localized nucleus Hep3B cells. The targeted expression conferred superior inhibitory activity on signaling, as determined reporter...