A5016021846- Inflammatory mediators and NSAID effects
- Peroxisome Proliferator-Activated Receptors
- Estrogen and related hormone effects
- Kruppel-like factors research
- Cancer, Lipids, and Metabolism
- Cancer, Hypoxia, and Metabolism
- Epigenetics and DNA Methylation
- Cancer-related gene regulation
- Pancreatic and Hepatic Oncology Research
- Genetic Syndromes and Imprinting
- Helicobacter pylori-related gastroenterology studies
- Veterinary medicine and infectious diseases
- Eicosanoids and Hypertension Pharmacology
- Cancer, Stress, Anesthesia, and Immune Response
- Immune cells in cancer
- Genomics, phytochemicals, and oxidative stress
- Synthesis of β-Lactam Compounds
- Galectins and Cancer Biology
- Pancreatitis Pathology and Treatment
- Metabolism, Diabetes, and Cancer
- Cancer Research and Treatments
- Wnt/β-catenin signaling in development and cancer
- Bioactive Compounds and Antitumor Agents
- Fatty Acid Research and Health
- Colorectal Cancer Screening and Detection
The University of Texas MD Anderson Cancer Center
2015-2024
Zhongnan Hospital of Wuhan University
2023
Wuhan University
2023
Xiangya Hospital Central South University
2017-2018
Central South University
2017-2018
The University of Texas Southwestern Medical Center
2011
Michael E. DeBakey VA Medical Center
2010
Qilu Hospital of Shandong University
2010
First Affiliated Hospital of Anhui Medical University
2008
Anhui Medical University
2008
Diminished apoptosis, a critical event in tumorigenesis, is linked to down-regulated 15-lipoxygenase-1 (15-LOX-1) expression colorectal cancer cells. 13-S-hydroxyoctadecadienoic acid (13-S-HODE), which the primary product of 15-LOX-1 metabolism linoleic acid, restores apoptosis. Nonsteroidal antiinflammatory drugs (NSAIDs) transcriptionally up-regulate induce Peroxisome proliferator-activated receptors (PPARs) are nuclear for and arachidonic metabolites. PPAR-delta promotes colonic...
Pancreatic intraepithelial neoplasia (PanIN) is a precursor of pancreatic ductal adenocarcinoma (PDAC), which commonly occurs in the general populations with aging. Although most PanIN lesions (PanINs) harbor oncogenic KRAS mutations that initiate tumorigenesis; PanINs rarely progress to PDAC. Critical factors promote this progression, especially targetable ones, remain poorly defined. We show peroxisome proliferator-activated receptor-delta (PPARδ), lipid nuclear receptor, upregulated...
Abstract KRAS mutations drive oncogenic alterations in numerous cancers, particularly human pancreatic ductal adenocarcinoma (PDAC). About 93% of PDACs have mutations, with G12D (∼42% cases) and G12V (∼32% being the most common. The recent approval sotorasib (AMG510), a small-molecule, covalent, selective KRASG12C inhibitor, for treating patients non–small cell lung cancer represents breakthrough targeted therapy. However, there is need to develop other much-needed KRAS-mutant inhibitors...
Peroxisome proliferator–activated receptor–δ (PPARD) is upregulated in many major human cancers, but the role that its expression cancer cells has metastasis remains poorly understood. Here, we show specific PPARD downregulation or genetic deletion of significantly repressed various models vivo. Mechanistically, promoted angiogenesis via interleukin 8 vivo and vitro. Analysis transcriptome profiling HCT116 colon with without gene patterns The Cancer Genome Atlas colorectal adenocarcinoma...
Abstract KLF4 and CD44 regulate cancer cell stemness, but their precise functions roles in metastatic progression are not well understood. In this study, we used both inducible genetic engineering approaches to assess whether the activities of these two factors intersect pancreatic cancer. We found that ablation Klf4 cells isolated from Klf4flox/flox mice drastically increased expression promoted acquisition stem-like properties, whereas tetracycline-inducible suppressed properties vitro...
Peroxisome proliferator–activated receptor-delta (PPAR-δ) is overexpressed in human colon cancer, but its contribution to colonic tumorigenesis controversial. We generated a mouse model which PPAR-δ was genetically disrupted epithelial cells by targeted deletion of exon 4. Elimination colon-specific expression confirmed real-time reverse transcription–polymerase chain reaction (real-time RT-PCR), immunoblotting, and activity assays. Mice with without genetic disruption (10–11 mice per group)...
Abstract APC mutations activate aberrant β-catenin signaling to drive initiation of colorectal cancer; however, cancer progression requires additional molecular mechanisms. PPAR-delta (PPARD), a downstream target β-catenin, is upregulated in cancer. However, promotion intestinal tumorigenesis following deletion PPARD Apcmin mice has raised questions about the effects on activation and In this study, we used mouse models overexpression or combined with mutation (ApcΔ580) epithelial cells...
Abstract Helicobacter pylori causes gastric inflammation, gland hyperplasia and is linked to cancer. Here, we studied the interplay between epithelial stem cells their stromal niche under homeostasis upon H. infection. We find that cell differentiation orchestrated by subsets of either produce BMP inhibitors in base, or ligands at surface. Exposure promotes a feed-forward loop inducing Bmp2 expression themselves, enforcing rapid lineage commitment terminally differentiated mucous pit cells....
Lipoxygenases (LOX) are key enzymes for the oxidative metabolism of polyunsaturated fatty acids into biologically active products. Clinical data on comparative levels various LOX products in tumorigenesis lacking. Therefore, we examined profiles several (5-LOX, 12-LOX, 15-LOX-1, and 15-LOX-2) by liquid chromatography/tandem mass spectrometry major steps colorectal (normal, polyp, cancer) a clinical study 125 subjects (49 with normal colon, 36 polyps, 40 who underwent prospective biopsies to...
The nuclear receptor peroxisome proliferator-activated receptor-δ/β (PPAR-d) is upregulated in human colorectal cancers, but its role colonic tumorigenesis remains controversial. We generated a novel mouse model of intestinally targeted PPAR-d overexpression to simulate upregulation colon carcinogenesis. Colon-specific was confirmed by real-time reverse transcription polymerase chain reaction, immunoblotting, and activity assays. Mice with without were tested for azoxymethane (AOM)–induced...
Purpose: The dismal prognosis of pancreatic cancer has been linked to poor tumor differentiation. However, molecular basis differentiation and potential therapeutic value the underlying molecules remain unknown. We investigated mechanistic underexpression Krüppel-like factor 4 (KLF4) in defined a novel epigenetic pathway its activation for treatment.Experimental Design: Expressions KLF4 DNMT1 tissues were determined by IHC genetic alterations KLF4's impact on examined using biology...
Transcriptional suppression of 15-lipoxygenase (LOX)-1 (15-LOX-1) helps enable human colorectal cancer cells escape apoptosis, a critical mechanism for colonic tumorigenesis. GATA-6 is strongly expressed in vitro cells; its down-regulation by pharmaceuticals associated with reversal 15-LOX-1 transcriptional suppression. The mechanistic contribution overexpression to tumorigenesis, especially concerning suppression, remains unknown. We tested whether differentially overexpressed cancers and...
See also: Commentaire de travail X. J. Xie et al., pp. 87Endoscopy 2011; 43(02): 172-173DOI: 10.1055/s-0031-1291812
Loss of terminal cell differentiation promotes tumorigenesis. 15-Lipoxygenase-1 (15-LOX-1) contributes to in normal cells. The mechanistic significance 15-LOX-1 expression loss human cancers suppression is unknown. In a screen 128 cancer lines representing more than 20 types cancer, we found that mRNA levels were markedly lower terminally differentiated Relative (relative the level primary human-derived bronchial epithelial cells) 79% screened relative p16 (INK4A), which and considered one...
Expression of 15-lipoxygenase-1 (15-LOX-1) is decreased in many human cancers; however, the mechanistic significance its expression has been difficult to determine because mouse homolog 12/15-LOX opposing functions. We generated a model which 15-LOX-1 transgene was targeted intestinal epithelium via villin promoter. Targeted confirmed by real-time reverse transcription–polymerase chain reaction and immunoblotting. When expressed colonic epithelial cells two independent lines (B6 FVB),...
The IL-6/signal transducer and activator of transcription 3 (STAT3) pathway is a critical signaling for colitis-associated colorectal cancer (CAC). Peroxisome proliferator-activated receptor (PPAR)-δ, lipid nuclear receptor, up-regulates IL-6. 15-Lipoxygenase-1 (15-LOX-1), which crucial to production mediators terminate inflammation, down-regulates PPAR-δ. 15-LOX-1 effects on IL-6/STAT3 CAC tumorigenesis have not been determined. We report that intestinally targeted transgenic expression in...