64 results on '"Qiangsheng, Hu"'
Search Results
52. FBW7-NRA41-SCD1 axis synchronously regulates apoptosis and ferroptosis in pancreatic cancer cells
- Author
-
Xiaowu Xu, Shunrong Ji, Yi Qin, Qifeng Zhuo, Xianjun Yu, Wenyan Xu, Qiangsheng Hu, Zeng Ye, Wensheng Liu, Mengqi Liu, Guixiong Fan, and Zheng Zhang
- Subjects
0301 basic medicine ,Programmed cell death ,F-Box-WD Repeat-Containing Protein 7 ,Clinical Biochemistry ,Cell ,Apoptosis ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Cell Line, Tumor ,Pancreatic cancer ,medicine ,Ferroptosis ,Humans ,Cytotoxic T cell ,lcsh:QH301-705.5 ,lcsh:R5-920 ,Chemistry ,Organic Chemistry ,Lipid metabolism ,medicine.disease ,Pancreatic Neoplasms ,Gene expression profiling ,030104 developmental biology ,medicine.anatomical_structure ,lcsh:Biology (General) ,FBW7 ,Cancer research ,lcsh:Medicine (General) ,Stearoyl-CoA Desaturase ,030217 neurology & neurosurgery ,TXNIP ,Research Paper - Abstract
FBW7 functions as a tumor suppressor by targeting oncoproteins for degradation. Our previous study found FBW7 was low expressed in pancreatic cancer due to sustained activation of Ras-Raf-MEK-ERK pathway, which destabilized FBW7 by phosphorylating at Thr205. MicroPET/CT imaging results revealed that FBW7 substantially decreased 18F-fluorodeoxyglucose uptake in xenograft tumors. Mechanistically, FBW7 inhibited glucose metabolism via c-Myc/TXNIP axis. But in these studies, we observed FBW7 down-regulated genes were widely involved in redox reaction and lipid metabolism. Here we reanalyzed previous gene expression profiling and conducted targeted cell metabolites analysis. Results revealed that FBW7 regulated lipid peroxidation and promoted ferroptosis, a non-apoptotic form of cell death. Mechanistically, we found FBW7 inhibited the expression of stearoyl-CoA desaturase (SCD1) via inhibiting nuclear receptor subfamily 4 group A member 1 (NR4A1). SCD1 was reported to inhibit both ferroptosis and apoptosis, which was consistent with the function of FBW7 and NR4A1, another FBW7 down-regulated gene in the gene expression profiling. Moreover, FBW7 potentiated cytotoxic effect of gemcitabine via activating ferroptosis and apoptosis. Combination ferroptosis inducers and apoptosis activators could also significantly potentiated cytotoxic effect of gemcitabine in pancreatic cancer. Therefore, our findings might provide new strategies for the comprehensive treatment of pancreatic cancer., Graphical abstract Image 1, Highlights • Ferroptosis possesses great potential in pancreatic cancer therapy. • FBW7 synchronously induces apoptosis and ferroptosis. • Activation of apoptosis and ferroptosis potentiates cytotoxic effect of gemcitabine.
- Published
- 2021
53. Homeodomain-interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer
- Author
-
Quanxing Ni, Bo Zhang, Weixing Dai, Xiaowu Xu, Jin Xu, Zheng Zhang, Wenyan Xu, Qiqing Sun, Shunrong Ji, Qiangsheng Hu, Wensheng Liu, Xianjun Yu, and Yi Qin
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,MAP Kinase Signaling System ,Protein Serine-Threonine Kinases ,Proto-Oncogene Proteins c-myc ,03 medical and health sciences ,0302 clinical medicine ,Pancreatic cancer ,Cell Line, Tumor ,medicine ,Humans ,Glycolysis ,Protein kinase A ,Cell Proliferation ,Cell growth ,Chemistry ,Protein Stability ,Cell Biology ,General Medicine ,Original Articles ,medicine.disease ,Prognosis ,Aerobiosis ,Gene Expression Regulation, Neoplastic ,Pancreatic Neoplasms ,030104 developmental biology ,Anaerobic glycolysis ,030220 oncology & carcinogenesis ,Cancer cell ,Cancer research ,Phosphorylation ,Carrier Proteins - Abstract
Objectives To investigate the roles of the homeodomain-interacting protein kinase (HIPK) family of proteins in pancreatic cancer prognosis and the possible molecular mechanism. Materials and methods The expression of HIPK family genes and their roles in pancreatic cancer prognosis were analysed by using The Cancer Genome Atlas (TCGA). The roles of HIPK2 in pancreatic cancer proliferation and glycolysis were tested by overexpression of HIPK2 in pancreatic cancer cells, followed by cell proliferation assay, glucose uptake analysis and Seahorse extracellular flux analysis. The mechanism of action of HIPK2 in pancreatic cancer proliferation and glycolysis was explored by examining its effect on the ERK/cMyc axis. Results Decreased HIPK2 expression indicated worse prognosis of pancreatic cancer. Overexpression of HIPK2 in pancreatic cancer cells decreased cell proliferation and attenuated aerobic glycolysis, which sustained proliferation of cancer cells. HIPK2 decreased cMyc protein levels and expression of cMyc-targeted glycolytic genes. cMyc was a mediator that regulated HIPK2-induced decrease in aerobic glycolysis. HIPK2 regulated cMyc protein stability via ERK activation, which phosphorylated and controlled cMyc protein stability. Conclusions HIPK2 suppressed proliferation of pancreatic cancer in part through inhibiting the ERK/cMyc axis and related aerobic glycolysis.
- Published
- 2018
54. An Integrated Approach to Evaluate Urban Adaptive Capacity to Climate Change
- Author
-
Qiangsheng Hu and Xiaorong He
- Subjects
010504 meteorology & atmospheric sciences ,Geography, Planning and Development ,Population ,TJ807-830 ,Climate change ,010501 environmental sciences ,Management, Monitoring, Policy and Law ,TD194-195 ,Urban area ,01 natural sciences ,urban area ,adaptive capacity ,climate change ,DPSIR ,GRA ,Renewable energy sources ,Urban planning ,Urbanization ,GE1-350 ,education ,Environmental planning ,0105 earth and related environmental sciences ,Sustainable development ,Adaptive capacity ,education.field_of_study ,geography.geographical_feature_category ,Environmental effects of industries and plants ,Renewable Energy, Sustainability and the Environment ,Environmental sciences ,Geography - Abstract
Climate change and accelerated urbanization have posed severe challenges to urban development, resulting in a growing series of climate and environmental problems that have a significant impact on industrial production and urban life. In a developing country such as China, more than 57% of the population lives in urban areas. It is vital for these cities to adapt to climate-induced risks. A better understanding of how to improve adaptive capacity could enhance the ability to achieve a desirable state when the city experiences stress. This paper used an integrated approach for evaluating the urban adaptive capacity to climate change. It developed the evaluation index system of urban adaptive capacity (UAC) based on the driver–pressure–state–impact–response model (DPSIR), and adopted grey relational analysis (GRA) and the entropy method to analyze the level of UAC in Changsha, the capital city of Hunan Province, from 2006 to 2015. The results revealed that the UAC of Changsha showed a significant increase from 2006 to 2015. Among the five first-grade indicators, the response dimension had the greatest influence on the improvement of UAC. The study may provide suggestions for adaptive capacity building and sustainable development in other urban areas.
- Published
- 2018
- Full Text
- View/download PDF
55. TCF7L2 positively regulates aerobic glycolysis via the EGLN2/HIF-1α axis and indicates prognosis in pancreatic cancer
- Author
-
Jin Xu, Jiang Liu, Shunrong Ji, Qiangsheng Hu, Wenyan Xu, Dingkong Liang, Wensheng Liu, Xianjun Yu, Jinfeng Xiang, Quanxing Ni, Yi Qin, Bo Zhang, Qingcai Meng, Chen Liang, and Si Shi
- Subjects
Male ,0301 basic medicine ,Cancer Research ,Transcription, Genetic ,Immunology ,medicine.disease_cause ,Article ,Hypoxia-Inducible Factor-Proline Dioxygenases ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,Hypoxia-Inducible Factor 1-Alpha ,0302 clinical medicine ,Fluorodeoxyglucose F18 ,Cell Line, Tumor ,Pancreatic cancer ,medicine ,Humans ,lcsh:QH573-671 ,Transcription factor ,Cell Proliferation ,Base Sequence ,Protein Stability ,lcsh:Cytology ,business.industry ,Wnt signaling pathway ,Cell Biology ,TCF4 ,Middle Aged ,Hypoxia-Inducible Factor 1, alpha Subunit ,Prognosis ,medicine.disease ,Survival Analysis ,Aerobiosis ,Pancreatic Neoplasms ,030104 developmental biology ,Hypoxia-inducible factors ,Anaerobic glycolysis ,030220 oncology & carcinogenesis ,Cancer research ,Female ,Carcinogenesis ,business ,Glycolysis ,Transcription Factor 7-Like 2 Protein ,Signal Transduction - Abstract
Patients with pancreatic ductal adenocarcinoma have much worse prognoses, and much effort has been directed toward understanding the molecular biological aspects of this disease. Accumulated evidence suggests that constitutive activation of the Wnt/β-catenin signalling contributes to the oncogenesis and progression of pancreatic cancer. Transcription factor 7-like2/transcription factor 4 (TCF7L2/TCF4), a β-catenin transcriptional partner, plays a vital role in the Wnt/β-catenin signalling pathway. In the present study, we investigated the clinicopathological significance of TCF7L2 in pancreatic cancer. Our results demonstrated that patients with higher TCF7L2 expression had worse prognosis. Our in vitro studies demonstrated that TCF7L2 positively regulated aerobic glycolysis by suppressing Egl-9 family hypoxia inducible factor 2 (EGLN2), leading to upregulation of hypoxia inducible factor 1 alpha subunit (HIF-1α). The impact of TCF7L2 on aerobic glycolysis was further confirmed in vivo by assessing 18FDG uptake in pancreatic cancer patients and in a subcutaneous xenograft mouse model. In summary, we identified novel predictive markers for prognosis and suggest a previously unrecognized role for TCF7L2 in control of aerobic glycolysis in pancreatic cancer.
- Published
- 2018
56. MBD1 promotes the malignant behavior of gallbladder cancer cells and induces chemotherapeutic resistance to gemcitabine
- Author
-
Wensheng, Liu, primary, Bo, Zhang, additional, Qiangsheng, Hu, additional, Wenyan, Xu, additional, Shunrong, Ji, additional, Jin, Xu, additional, Quanxing, Ni, additional, Xianjun, Yu, additional, and Xiaowu, Xu, additional
- Published
- 2019
- Full Text
- View/download PDF
57. A new facet of NDRG1 in pancreatic ductal adenocarcinoma: Suppression of glycolytic metabolism
- Author
-
Quanxing Ni, Pengfei Hu, Jiang Long, Liang Liu, Yi Qin, Shunrong Ji, Wensheng Liu, Jin Xu, Jinfeng Xiang, Qiangsheng Hu, Qingcai Meng, Dingkong Liang, Chen Liang, Chen Liu, Bo Zhang, Xianjun Yu, Jiang Liu, Wenyan Xu, and Si Shi
- Subjects
0301 basic medicine ,Male ,Cancer Research ,Angiogenesis ,MAP Kinase Signaling System ,Cell Cycle Proteins ,Biology ,Adenocarcinoma ,Metastasis ,03 medical and health sciences ,Pancreatic cancer ,Cell Line, Tumor ,medicine ,Humans ,Metastasis suppressor ,Genes, Tumor Suppressor ,Neoplasm Metastasis ,Protein kinase B ,Intracellular Signaling Peptides and Proteins ,Cancer ,medicine.disease ,Hypoxia-Inducible Factor 1, alpha Subunit ,Neoplasm Proteins ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Oncology ,Anaerobic glycolysis ,Cancer cell ,Cancer research ,Female ,Glycolysis ,Carcinoma, Pancreatic Ductal - Abstract
N-myc downstream-regulated gene 1 (NDRG1) is known as tumor/metastasis suppressor in a variety of cancers including pancreas, being involved in angiogenesis, cancer growth and metastasis. However, the precise molecular mechanism how NDRG1 exerts its inhibitory function in pancreatic cancer remains unclear. In this investigation, we demonstrated that K-Ras plays a vital role in modulating NDRG1 protein level in PDAC cancer cells in vitro, which is mediated through ERK signaling. Noteworthy, K-Ras downstream Akt/mTOR signaling is inhibited upon NDRG1 overexpression, resulting in decease of HIF1α level. Moreover, NDRG1 has a unique role in modulating cancer metabolism of pancreatic ductal adenocarcinoma (PDAC). The mechanism accounting for NDRG1 in modulating aerobic glycolysis, at least partly, relied on its regulation of glycolysis genes including GLUT1, HK2, LDHA and PDK1. Additionally, NDRG1 is shown to suppress the activity of HIF1α, which is responsible for regulation of glycolysis enzymes. The current study is the first to elucidate a unique facet of the potent tumor/metastasis suppressor NDRG1 in the regulation of PDAC glycolysis, leading to important insights into the mechanism by which NDRG1 exert inhibitory function in PDAC.
- Published
- 2016
58. Oncogenic KRAS Targets MUC16/CA125 in Pancreatic Ductal Adenocarcinoma
- Author
-
Bo Zhang, Qiangsheng Hu, Dingkong Liang, Wenyan Xu, Xianjun Yu, Si Shi, Quanxing Ni, Chen Liang, Yi Qin, Shunrong Ji, Jinfeng Xiang, Jin Xu, and Jiang Liu
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Cancer Research ,endocrine system diseases ,Mice, Transgenic ,Biology ,medicine.disease_cause ,Transfection ,Proto-Oncogene Mas ,Proto-Oncogene Proteins p21(ras) ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Downregulation and upregulation ,Pancreatic cancer ,Cell Line, Tumor ,Proto-Oncogenes ,medicine ,Carcinoma ,Animals ,Humans ,Promoter Regions, Genetic ,Survival rate ,Molecular Biology ,Membrane Proteins ,medicine.disease ,Pancreatic Neoplasms ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,CA-125 Antigen ,Cancer research ,CA19-9 ,KRAS ,Carcinoma, Pancreatic Ductal - Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with the 5-year survival rate less than 6%. Previous results indicated that serum levels of CA125 (encoded by MUC16) could be used to predict which groups of pancreatic cancer patients may benefit from surgery. However, the underlying mechanism remains elusive. Herein, using the Cancer Genome Atlas and clinicopathologic data obtained from our center, we demonstrate that high CA125 serum levels and expression levels of MUC16 are predictive of poor prognosis. MUC16 is also validated as a downstream target of KRAS, and their expression strongly correlated with each other in vitro and in vivo. Mechanistically, the KRAS/ERK axis induced upregulation of MUC16 and shedding of CA125 via its effector c-Myc in SW1990 and PANC-1 pancreatic cancer cells. Notably, proto-oncogene c-Myc could bind to the promoter of MUC16 and transcriptionally activate its expression. Taken together, these data establish CA125 as a prognostic marker for pancreatic cancer, and mechanistic studies uncovered the KRAS/c-Myc axis as a driving factor for upregulation of MUC16. Implications: The current study uncovers the contribution of oncogenic KRAS to serum marker CA125 production through a mechanism that involves the ERK/c-Myc axis. Mol Cancer Res; 15(2); 201–12. ©2016 AACR.
- Published
- 2016
59. Metabolic plasticity in heterogeneous pancreatic ductal adenocarcinoma
- Author
-
Yi Qin, Quanxing Ni, Xianjun Yu, Chen Liang, Si Shi, Jin Xu, Jiang Liu, Bo Zhang, Wenyan Xu, Shunrong Ji, Jinfeng Xiang, Qiangsheng Hu, and Dingkong Liang
- Subjects
0301 basic medicine ,Cancer Research ,Stromal cell ,education ,Biology ,Bioinformatics ,law.invention ,Proto-Oncogene Proteins c-myc ,Proto-Oncogene Proteins p21(ras) ,03 medical and health sciences ,0302 clinical medicine ,law ,Pancreatic cancer ,Genetics ,medicine ,Tumor Microenvironment ,Animals ,Humans ,Glycolysis ,Lipid metabolism ,medicine.disease ,Glutamine ,Pancreatic Neoplasms ,Metabolic pathway ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,Cancer cell ,Cancer research ,Suppressor ,Stromal Cells ,Tumor Suppressor Protein p53 ,Carcinoma, Pancreatic Ductal - Abstract
Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal malignant neoplasms. The recognized hallmarks of PDA are regarded to be downstream events of metabolic reprogramming. Because PDA is a heterogeneous disease that is influenced by genetic polymorphisms and changes in the microenvironment, metabolic plasticity is a novel feature of PDA. As intrinsic factors for metabolic plasticity, K-ras activation and mutations in other tumor suppressor genes induce abnormal mitochondrial metabolism and enhance glycolysis, with alterations in glutamine and lipid metabolism. As extrinsic factors, the acidic and oxygen/nutrient-deprived microenvironment also induces cancer cells to reprogram their metabolic pathway and hijack stromal cells (mainly cancer-associated fibroblasts and immunocytes) to communicate, thereby adapting to metabolic stress. Therefore, a better understanding of the metabolic features of PDA will contribute to the development of novel diagnostic and therapeutic strategies.
- Published
- 2016
60. dCK negatively regulates the NRF2/ARE axis and ROS production in pancreatic cancer
- Author
-
Quanxing Ni, Qiqing Sun, Jiang Liu, Yi Qin, Bo Zhang, Wenyan Xu, Jin Xu, Shunrong Ji, Xianjun Yu, Wensheng Liu, Jinfeng Xiang, Zheng Zhang, and Qiangsheng Hu
- Subjects
0301 basic medicine ,Cell Survival ,NF-E2-Related Factor 2 ,Glutamate-Cysteine Ligase ,dCK ,pancreatic cancer ,Deoxycytidine ,NRF2 ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Cell Line, Tumor ,Pancreatic cancer ,Deoxycytidine Kinase ,medicine ,Humans ,Transcription factor ,Cell Proliferation ,Mitogen-Activated Protein Kinase 1 ,Kelch-Like ECH-Associated Protein 1 ,Mitogen-Activated Protein Kinase 3 ,Cell growth ,Chemistry ,Kinase ,gemcitabine ,ROS ,Original Articles ,Cell Biology ,General Medicine ,Deoxycytidine kinase ,medicine.disease ,Glutathione ,NFE2L2 ,ARE ,Acetylcysteine ,Up-Regulation ,Pancreatic Neoplasms ,030104 developmental biology ,Drug Resistance, Neoplasm ,030220 oncology & carcinogenesis ,Cancer research ,Original Article ,Reactive Oxygen Species ,Intracellular ,Plasmids - Abstract
Objectives Decreased deoxycytidine kinase (dCK) expression is a reported indicator of gemcitabine efficacy in pancreatic cancer, due to the impact of this kinase on gemcitabine metabolism. The transcription factor NF‐E2 p45‐related factor 2 (NRF2, also called Nfe2l2), a master regulator of redox homoeostasis, has been reported to tightly control the expression of numerous ROS‐detoxification genes and participates in drug resistance. However, the contribution of dCK to the NRF2 signalling axis has seldom been discussed and needs investigation. Materials and methods By overexpressing dCK in pancreatic cancer cells, we assessed the impact of dCK on NRF2 transcriptional activity. Furthermore, we measured the impact of dCK expression on the intracellular redox balance and reactive oxygen species (ROS) production. By utilizing immunohistochemical staining and tissues from pancreatic cancer patients, we assessed the correlation between dCK and NRF2 expression. Through proliferation and metastasis assays, we examined the impact of dCK expression on cell proliferation and metastasis. Results dCK negatively regulates NRF2 transcriptional activity, leading to the decreased expression of ARE‐driven antioxidant genes. In addition, dCK negatively regulates intracellular redox homoeostasis and ROS production. Negative correlations between dCK and NRF2 levels in pancreatic cancer cell lines and patient samples were observed. In vitro cell line studies suggested that dCK negatively regulated proliferation and metastasis. Conclusion Decreased dCK expression promotes NRF2‐driven antioxidant transcription, which further enhances gemcitabine treatment resistance, forming a feedback loop.
- Published
- 2018
61. FBW7 increases the chemosensitivity of pancreatic cancer cells to gemcitabine through upregulation of ENT1.
- Author
-
QIANGSHENG HU, YI QIN, BO ZHANG, CHEN LIANG, SHUNRONG JI, SI SHI, WENYAN XU, JINFENG XIANG, DINGKONG LIANG, QUANXING NI, XIANJUN YU, and JIN XU
- Published
- 2017
- Full Text
- View/download PDF
62. Fabrication of Yb3+-doped photonic crystal fibers
- Author
-
Guiyao Zhou, Changmin Xia, Wei Zhang, and Qiangsheng Hu
- Published
- 2012
63. A new facet of NDRG1 in pancreatic ductal adenocarcinoma: Suppression of glycolytic metabolism.
- Author
-
WENSHENG LIU, BO ZHANG, QIANGSHENG HU, YI QIN, WENYAN XU, SI SHI, CHEN LIANG, QINGCAI MENG, JINFENG XIANG, DINGKONG LIANG, SHUNRONG JI, JIANG LIU, PENGFEI HU, LIANG LIU, CHEN LIU, JIANG LONG, QUANXING NI, XIANJUN YU, and JIN XU
- Published
- 2017
- Full Text
- View/download PDF
64. Energy sources identify metabolic phenotypes in pancreatic cancer.
- Author
-
Chen Liang, Yi Qin, Bo Zhang, Shunrong Ji, Si Shi, Wenyan Xu, Jiang Liu, Jinfeng Xiang, Dingkong Liang, Qiangsheng Hu, Liang Liu, Chen Liu, Guopei Luo, Quanxing Ni, Jin Xu, and Xianjun Yu
- Published
- 2016
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.