A5065938903- Phagocytosis and Immune Regulation
- Cancer Cells and Metastasis
- Epigenetics and DNA Methylation
- Bladder and Urothelial Cancer Treatments
- Cancer Research and Treatments
- Cell death mechanisms and regulation
- Kruppel-like factors research
- Erythrocyte Function and Pathophysiology
- Immune responses and vaccinations
- CRISPR and Genetic Engineering
- RNA Research and Splicing
- RNA modifications and cancer
- Immune cells in cancer
- Cancer Mechanisms and Therapy
- Cancer, Lipids, and Metabolism
- Renal and related cancers
- Mitochondrial Function and Pathology
- Microtubule and mitosis dynamics
- Signaling Pathways in Disease
- interferon and immune responses
- Peptidase Inhibition and Analysis
- PARP inhibition in cancer therapy
- Science, Research, and Medicine
- RNA Interference and Gene Delivery
- Cancer Immunotherapy and Biomarkers
Moffitt Cancer Center
2018-2024
Molecular Oncology (United States)
2018-2024
The University of Texas MD Anderson Cancer Center
2010-2017
Canadian Institutes of Health Research
2016
Rajiv Gandhi Centre for Biotechnology
2008
Cancer cells require both migratory and tumorigenic property to establish metastatic tumors outside the primary microenvironment. Identifying characteristic features of cancer stem with is important predict patient prognosis combat metastasis. Here we established one epithelial two mesenchymal cell lines from ascites a bladder (i.e. already migrated tumor). Analyses these demonstrated that surface expression PD-L1, E-cadherin, CD24, VEGFR2 rapidly formed tumor microenvironment in nude mice,...
Triple negative breast cancers (TNBCs) are known to express low PGR, ESR1, and ERBB2, high KRT5, KRT14, KRT17. However, the reasons behind increased expressions of KRT17 decreased ERBB2 in TNBCs not fully understood. Here we show that, expression chromosome 19 miRNA cluster (C19MC) specifically marks human TNBCs. Low REST CEBPB correlate with C19MC, enhancers these genes/cluster regulated by binding sites. The C19MC miRNAs turn can potentially target offer a positive feedback loop, might...
Abstract Smac mimetic overcomes resistance of bladder cancer cells to BCG-stimulated neutrophils through TNF-α. BCG, the current gold standard immunotherapy for cancer, exerts its activity via recruitment tumor microenvironment. Many patients do not respond BCG therapy, indicating need understand mechanism action and identify ways overcome therapy. Using isolated human stimulated with we found that TNF-α is key mediator secreted by neutrophils. RT4v6 cells, which express TNFR1, CD95/Fas,...
The blebbishield emergency program helps to resurrect apoptotic cancer stem cells (CSCs) themselves. Understanding the mechanisms behind this is essential block resurrection of CSCs during therapy. Here we demonstrate that endocytosis drives serpentine filopodia construct blebbishields from bodies and a VEGF-VEGFR2-endocytosis-p70S6K axis governs subsequent transformation. Disengagement RalGDS E-cadherin initiates its novel interaction partners cdc42, VEGFR2, cleaved β-catenin, PKC-ζ as well...
Undifferentiated embryonal sarcoma of the liver (UESL) is a rare and aggressive malignancy. Though molecular underpinnings this cancer have been largely unexplored, recurrent chromosomal breakpoints affecting noncoding region on chr19q13, which includes chromosome 19 microRNA cluster (C19MC), reported in several cases. We performed comprehensive profiling samples from 14 patients diagnosed with UESL. Congruent prior reports, we identified structural variants chr19q13 10 13 evaluable tumors....
Purpose: Inhibitors of apoptosis proteins (IAPs) have been shown to contribute resistance neoplastic cells chemotherapy and biologic antineoplastic agents. Consequently, new agents are being developed targeting this family proteins. In a panel bladder cancer cell lines, we evaluated Smac mimetic that antagonizes several IAPs for its suitability therapy.
Intravesical bacillus Calmette-Guérin (BCG) immunotherapy results in neutrophil recruitment and subsequent secretion of cytokines to eliminate non-muscle invasive bladder cancer cells. However, cells often resist BCG immunotherapy. Thus, understanding the mechanism action BCG, designing appropriate combination therapies might help overcome resistance redirect neutrophils against
Abstract Cancer stem cells are capable of transformation after apoptosis through the blebbishield emergency program. Reactive oxygen species (ROS) play an essential role in transformation. Understanding how ROS linked to blebbishield-mediated is necessary develop efficient therapeutics that target resurrection cancer cells. Here we demonstrate a novel PKC-ζ p47 phox interaction required for production The combined use S6K inhibitor BI-D1870 with TNF-α inhibited interaction, production,...
Cancer cells are capable of sphere formation (transformation) through reactive oxygen species (ROS) and glycolysis shift. Transformation is linked to tumorigenesis therapy resistance, hence targeting regulators ROS important for cancer therapeutic candidates. Here, we demonstrate that Smac mimetic AZ58 in combination with tumour necrosis factor-α (TNF-α) was able inhibit the production ROS, Pim-1 kinase-mediated Ser-112 phosphorylation BAD, increase depolarization mitochondria. We also...
Cisplatin-based chemotherapy is considered the gold standard for patients with advanced bladder cancer. However, despite initial response, many will relapse; therefore, novel salvage treatment strategies are desperately needed. Herein, we studied a mechanism based combination using Smac mimetic chemotherapy. Using panel of 10 urothelial cancer cell lines, exposed them to gemcitabine, cisplatin, and mimetic. Sensitivity was determined DNA fragmentation assay. We that three lines (UMUC-3,...
Cancer stem cells evade apoptotic death by blebbishield emergency program, which constructs blebbishields from bodies and drives cellular transformation. Von Hippel-Lindau (VHL) plays both tumor suppressor oncogenic roles, the reason behind is poorly understood. Here we demonstrate that dimers trimers of p19-VHL interact with RalBP1 to construct blebbishields. Expression RalBP1, p19-VHL, high-molecular weight VHL required apoptosis blebbishield-mediated In contrast, p30-VHL a role inhibiting...
Genomic instability and immune evasion are hallmarks of cancer. Apoptotic cancer stem cells can evade cell death by undergoing cellular transformation constructing "blebbishields" from apoptotic bodies. In this study, we report a novel linkage between genomic phagocytosis that is coordinated the blebbishield emergency program. Blebbishield program evaded checkpoint, expressed instability-associated genes at distinct phases transformation, exhibited chromosomal instability, promoted increase...