A5013946172- Chemokine receptors and signaling
- Cancer, Stress, Anesthesia, and Immune Response
- Cancer, Hypoxia, and Metabolism
- Cancer, Lipids, and Metabolism
- Inflammatory mediators and NSAID effects
- Prostate Cancer Treatment and Research
- PI3K/AKT/mTOR signaling in cancer
- Cancer-related molecular mechanisms research
- Genomics, phytochemicals, and oxidative stress
- Cholinesterase and Neurodegenerative Diseases
- Fungal Plant Pathogen Control
- Cell Adhesion Molecules Research
- Cancer-related Molecular Pathways
- Nitric Oxide and Endothelin Effects
- Eicosanoids and Hypertension Pharmacology
- Ferroptosis and cancer prognosis
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Bone health and treatments
- Immune cells in cancer
- Redox biology and oxidative stress
- Cytokine Signaling Pathways and Interactions
- Cancer Cells and Metastasis
- Receptor Mechanisms and Signaling
- Angiogenesis and VEGF in Cancer
- RNA modifications and cancer
Clark Atlanta University
2014-2024
Center for Cancer Research
2011-2023
Clark University
2020-2021
Georgia Institute of Technology
2010
Beth Israel Deaconess Medical Center
2007-2008
Harvard University
2007
Meharry Medical College
2007
Background While vascular endothelial growth factor (VEGF) expression in breast tumors has been correlated with a poor outcome the pathogenesis of cancer, expression, localization, and function VEGF receptors VEGFR1 (also known as FLT1) VEGFR2 KDR or FLK1), well neuropilin 1 (NRP1), cancer are controversial. Methods Findings We investigated cells. observed that was abundant, low, NRP1 variable. MDA-MB-231 MCF-7 cells, transfected antisense cDNA siVEGF (VEGF-targeted small interfering RNA),...
Abstract Inadequate nutrient intake leads to oxidative stress disrupting homeostasis, activating signaling, and altering metabolism. Oxidative serves as a hallmark in developing prostate lesions, an aggressive cancer phenotype mechanisms allowing cells adapt survive. It is unclear how adaptation survival are facilitated; however, literature across several organisms demonstrates that reversible cellular growth arrest the transcription factor, nuclear factor-kappaB (NF-κB), contribute cell...
The G-protein coupled receptor (GPCR), Cysteine (C)-X-C Receptor 4 (CXCR4), plays an important role in prostate cancer metastasis. CXCR4 is generally regarded as a plasma membrane where it transmits signals that support transformation, progression and eventual Due to the central of tumorigenesis, therapeutics approaches such antagonist monoclonal antibodies have focused on receptors exist membrane. An emerging concept for they may localize associate with nucleus retain function mediate...
Peroxidasin (PXDN), a human homolog of Drosophila PXDN, belongs to the family heme peroxidases and has been found promote oxidative stress in cardiovascular tissue, however, its role prostate cancer not previously elucidated. We hypothesized that PXDN promotes progression via regulation metabolic pathways. analyzed expression tissue by immunohistochemistry increased with as compared normal or cells. knockdown followed proteomic analysis revealed an increase stress, mitochondrial dysfunction...
Loss of PTEN is frequently observed in androgen-independent prostate cancer, resulting the deregulation metastatic events. SDF1α activation CXCR4 induces signaling pathways that have been implicated metastasis and progression to an advanced disease. The converge, leading promotion regulation tumorigenesis, respectively. However, loss may permit progress cancer In present study, we investigated involvement CXCR4-mediated tumorigenesis. When screening cell lines for PTEN, a expression PC3...
G-protein-coupled receptor (GPCR) heterodimerization has emerged as a means by which alternative signaling entities can be created; yet, how heterodimers affect pharmacology remains unknown. Previous observations suggested biochemical antagonism between GPCRs, CXCR4 and CB2 (CNR2), where agonist-bound formed physiologically nonfunctional heterodimer on the membrane of cancer cells, inhibiting their metastatic potential in vitro However, reduced responsible for observed functional outputs...
Abstract BACKGROUND Bone marrow stromal cell (BMSC) paracrine factor(s) can induce apoptosis in bone metastatic prostate cancer (PCa) lines. However, the PCa cells that escape BMSC‐induced upregulate cytoprotective autophagy. METHODS C4‐2, C4‐2B, MDA 2a, 2b, VCaP, PC3, or DU145 lines were grown BMSC conditioned medium and analyzed for mRNA and/or protein accumulation of p62 (also known as sequestome‐1/SQSTM1), Microtubule‐associated 1 light chain 3B (LC3B), lysosomal‐associated membrane...
Camalexin, the phytoalexin produced in model plant Arabidopsis thaliana, possesses antiproliferative and cancer chemopreventive effects. We have demonstrated that cytostatic/cytotoxic effects of camalexin on several prostate (PCa) cells are due to oxidative stress. Lysosomes vulnerable organelles Reactive Oxygen Species (ROS)-induced injuries, with potential initiate or facilitate apoptosis subsequent release proteases such as cathepsin D (CD) into cytosol. therefore hypothesized reduces...
Chemoresistance is a major obstacle in the clinical management of metastatic, castration-resistant prostate cancer (PCa). It imperative to develop novel strategies overcome chemoresistance and improve outcomes patients who have failed chemotherapy. Using two-tier phenotypic screening platform, we identified bromocriptine mesylate as potent selective inhibitor chemoresistant PCa cells. Bromocriptine effectively induced cell cycle arrest activated apoptosis cells but not chemoresponsive...
This paper details U.S. Research Centers in Minority Institutions (RCMI) Community Engagement Cores (CECs): (1) unique and cross-cutting components, focus areas, specific aims, target populations; (2) approaches utilized to build or sustain trust towards community participation research. A mixed-method data collection approach was employed for this cross-sectional study of current previously funded RCMIs. total 18 the 25 institutions spanning 13 states territories participated. CEC aims were...
Oxidative stress is increased in several cancers including prostate cancer, and currently being exploited cancer therapy to induce ferroptosis, a novel nonapoptotic form of cell death. High mobility group A2 (HMGA2), non-histone protein up-regulated cancers, can be truncated due chromosomal rearrangement or alternative splicing HMGA2 gene. The purpose this study investigate the role wild-type vs. (PCa). We analyzed expression showed that patient tissue some lines expressed increasing amounts...
Funded by the National Institutes of Health (NIH), Research Centers in Minority Institutions (RCMI) Program fosters development and implementation innovative research aimed at improving minority health reducing or eliminating disparities. Currently, there are 21 RCMI Specialized (U54) that share same framework, comprising four required core components, namely Administrative, Infrastructure, Investigator Development, Community Engagement Cores. The Infrastructure Core (RIC) is fundamentally...
Abstract The G-protein-coupled chemokine receptor (GPCR), CXCR4, is ubiquitously expressed in malignant tumor tissues, and controls migration other survival mechanisms upon interaction with its agonist, stromal cell-derived 1α (SDF1α). CXCR4/SDF1α axis relevant to shaping the microenvironment mainly metastatic spread of primary tumors distal organs immune response; thus, expression CXCR4 vital aggressiveness, probability, metastasis-associated mortality. signals through a homodimer, but also...
Abstract Cellular oxidative stress is one of the several hallmarks aggressive phenotypes observed in prostate cancer. As levels reactive oxygen species (ROS) increase, stressors activate mechanisms allowing cancer cells to adapt and survive. It unclear how survive stress; however, literature demonstrates that transcription factor, nuclear factor-kappa B (NF-κB) contributes survival during stress. In cancer, factors resulting stress, including chemotherapy, correlate with NF-κB expression...