scholarly journals Tumor Protein D52 (TPD52) Affects Cancer Cell Metabolism by Negatively Regulating AMPK

2019 ◽  
Author(s):  
Yali Chen ◽  
Yuanyuan Zhao ◽  
Pei Jiang ◽  
Wei Tan ◽  
Jia Yu ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Cell Metabolism ◽  
Cancer Cell Metabolism

scholarly journals A Holistic Evolutionary and 3D Pharmacophore Modelling Study Provides Insights into the Metabolism, Function, and Substrate Selectivity of the Human Monocarboxylate Transporter 4 (hMCT4)

2021 ◽  
Vol 22 (6) ◽  
pp. 2918
Author(s):  
Eleni Papakonstantinou ◽  
Dimitrios Vlachakis ◽  
Trias Thireou ◽  
Panayiotis G. Vlachoyiannopoulos ◽  
Elias Eliopoulos
Keyword(s):  
Cancer Cell ◽  
Structural Characteristics ◽  
Cell Metabolism ◽  
Intracellular Localization ◽  
Selective Inhibition ◽  
Monocarboxylate Transporter ◽  
Cancer Drug ◽  
Pharmacophore Modelling ◽  
Anti Cancer ◽  
Cancer Cell Metabolism

Monocarboxylate transporters (MCTs) are of great research interest for their role in cancer cell metabolism and their potential ability to transport pharmacologically relevant compounds across the membrane. Each member of the MCT family could potentially provide novel therapeutic approaches to various diseases. The major differences among MCTs are related to each of their specific metabolic roles, their relative substrate and inhibitor affinities, the regulation of their expression, their intracellular localization, and their tissue distribution. MCT4 is the main mediator for the efflux of L-lactate produced in the cell. Thus, MCT4 maintains the glycolytic phenotype of the cancer cell by supplying the molecular resources for tumor cell proliferation and promotes the acidification of the extracellular microenvironment from the co-transport of protons. A promising therapeutic strategy in anti-cancer drug design is the selective inhibition of MCT4 for the glycolytic suppression of solid tumors. A small number of studies indicate molecules for dual inhibition of MCT1 and MCT4; however, no selective inhibitor with high-affinity for MCT4 has been identified. In this study, we attempt to approach the structural characteristics of MCT4 through an in silico pipeline for molecular modelling and pharmacophore elucidation towards the identification of specific inhibitors as a novel anti-cancer strategy.

scholarly journals Oncolytic Virotherapy: The Cancer Cell Side

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 939
Author(s):  
Marcelo Ehrlich ◽  
Eran Bacharach
Keyword(s):  
Viral Replication ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Tumor Development ◽  
Oncolytic Viruses ◽  
Oncogenic Signaling ◽  
Functional Connection ◽  
Immunity Genes ◽  
Cancer Cell Metabolism ◽  
Editing Process

Cell autonomous immunity genes mediate the multiple stages of anti-viral defenses, including recognition of invading pathogens, inhibition of viral replication, reprogramming of cellular metabolism, programmed-cell-death, paracrine induction of antiviral state, and activation of immunostimulatory inflammation. In tumor development and/or immunotherapy settings, selective pressure applied by the immune system results in tumor immunoediting, a reduction in the immunostimulatory potential of the cancer cell. This editing process comprises the reduced expression and/or function of cell autonomous immunity genes, allowing for immune-evasion of the tumor while concomitantly attenuating anti-viral defenses. Combined with the oncogene-enhanced anabolic nature of cancer-cell metabolism, this attenuation of antiviral defenses contributes to viral replication and to the selectivity of oncolytic viruses (OVs) towards malignant cells. Here, we review the manners by which oncogene-mediated transformation and tumor immunoediting combine to alter the intracellular milieu of tumor cells, for the benefit of OV replication. We also explore the functional connection between oncogenic signaling and epigenetic silencing, and the way by which restriction of such silencing results in immune activation. Together, the picture that emerges is one in which OVs and epigenetic modifiers are part of a growing therapeutic toolbox that employs activation of anti-tumor immunity for cancer therapy.

AVB-500, a selective inhibitor of GAS6-AXL, in combination with paclitaxel alters uterine serous cancer cell metabolism

2021 ◽  
Vol 162 ◽  
pp. S97
Author(s):  
Shaina Bruce ◽  
Kevin Cho ◽  
Elena Lomonosova ◽  
Hollie Noia ◽  
Elizabeth Stock ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Cell Metabolism ◽  
Selective Inhibitor ◽  
Cancer Cell Metabolism

scholarly journals Collagen density modulates triple-negative breast cancer cell metabolism through adhesion-mediated contractility

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Emma J. Mah ◽  
Austin E. Y. T. Lefebvre ◽  
Gabrielle E. McGahey ◽  
Albert F. Yee ◽  
Michelle A. Digman
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Cell Metabolism ◽  
Cancer Cell Metabolism ◽  
Collagen Density

Apoptosis triggered by isoquercitrin in bladder cancer cells by activating the AMPK-activated protein kinase pathway

2017 ◽  
Vol 8 (10) ◽  
pp. 3707-3722 ◽  
Author(s):  
Ping Wu ◽  
Siyuan Liu ◽  
Jianyu Su ◽  
Jianping Chen ◽  
Lin Li ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Bladder Cancer Cell ◽  
Bladder Cancer Cells ◽  
Immunoblotting Assay ◽  
Cancer Cell Metabolism ◽  
Kinase Pathway

Our findings provide comprehensive evidence that isoquercitrin (ISO) influenced T24 bladder cancer cell metabolism by activating the AMPK pathway as identified by combination with metabolomics and immunoblotting assay.

scholarly journals The Neglected Liaison: Targeting Cancer Cell Metabolic Reprogramming Modifies the Composition of Non-Malignant Populations of the Tumor Microenvironment

Cancers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 5447
Author(s):  
Maria Iorio ◽  
Nikkitha Umesh Ganesh ◽  
Monica De Luise ◽  
Anna Maria Porcelli ◽  
Giuseppe Gasparre ◽  
...  
Keyword(s):  
Complex System ◽  
Clinical Trials ◽  
Cancer Cell ◽  
Immune Cells ◽  
Cell Metabolism ◽  
Metabolic Reprogramming ◽  
Preclinical Studies ◽  
Tumor Mass ◽  
Cancer Cell Metabolism ◽  
Target Cancer

Metabolic reprogramming is a well-known hallmark of cancer, whereby the development of drugs that target cancer cell metabolism is gaining momentum. However, when establishing preclinical studies and clinical trials, it is often neglected that a tumor mass is a complex system in which cancer cells coexist and interact with several types of microenvironment populations, including endothelial cells, fibroblasts and immune cells. We are just starting to understand how such populations are affected by the metabolic changes occurring in a transformed cell and little is known

scholarly journals Cross-Talk between Alternatively Spliced UGT1A Isoforms and Colon Cancer Cell Metabolism

2017 ◽  
Vol 91 (3) ◽  
pp. 167-177 ◽  
Author(s):  
Yannick Audet-Delage ◽  
Michèle Rouleau ◽  
Mélanie Rouleau ◽  
Joannie Roberge ◽  
Stéphanie Miard ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cell ◽  
Cross Talk ◽  
Cell Metabolism ◽  
Colon Cancer Cell ◽  
Alternatively Spliced ◽  
Cancer Cell Metabolism

scholarly journals Targeting cancer cell metabolism with mitochondria-immobilized phosphorescent cyclometalated iridium(iii) complexes

2017 ◽  
Vol 8 (1) ◽  
pp. 631-640 ◽  
Author(s):  
Jian-Jun Cao ◽  
Cai-Ping Tan ◽  
Mu-He Chen ◽  
Na Wu ◽  
De-Yang Yao ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Rational Design ◽  
Cell Metabolism ◽  
Mitochondrial Metabolism ◽  
Cancer Cell Metabolism

We report a rational design and mechanism studies of mitochondria-immobilized iridium(iii) complexes that can kill cancer cells by targeting mitochondrial metabolism.

Roles of microRNA in prostate cancer cell metabolism

2018 ◽  
Vol 102 ◽  
pp. 109-116 ◽  
Author(s):  
Khanmi Kasomva ◽  
Arnab Sen ◽  
Michael Gabriel Paulraj ◽  
Stephen Sailo ◽  
Vandana Raphael ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cell Metabolism ◽  
Cancer Cell Metabolism

Regulation of Cancer Cell Metabolism by Hypoxia

2014 ◽  
pp. 75-108
Author(s):  
Ashleigh Pulkoski-Gross ◽  
Nikki A. Evensen ◽  
Jian Cao
Keyword(s):  
Cancer Cell ◽  
Cell Metabolism ◽  
Cancer Cell Metabolism
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