scholarly journals MicroRNA‑513a‑3p regulates colorectal cancer cell metabolism via targeting hexokinase 2

2020 ◽  
Vol 20 (1) ◽  
pp. 572-580
Author(s):  
Chen Li ◽  
Zhijin Yu ◽  
Jinpeng Ye
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Colorectal Cancer Cell ◽  
Hexokinase 2 ◽  
Cancer Cell Metabolism

scholarly journals Targeting colorectal cancer cell metabolism through development of cisplatin and metformin nano-cubosomes

BMC Cancer ◽  
2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Mona M. Saber ◽  
Abdulaziz M. Al-mahallawi ◽  
Noha N. Nassar ◽  
Björn Stork ◽  
Samia A. Shouman
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Colorectal Cancer Cell ◽  
Cancer Cell Metabolism

scholarly journals USP28 promotes aerobic glycolysis of colorectal cancer by increasing stability of FOXC1

2021 ◽  
Author(s):  
Zhaohui Liu ◽  
Min Chen ◽  
Xiaoping Xu ◽  
Lei Zhang ◽  
Yuan Pan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
Aerobic Glycolysis ◽  
Cell Metabolism ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Over Expression ◽  
Cancer Cell Metabolism ◽  
Cancer Tissues

Aerobic glycolysis is essential for cancer cell metabolism and growth. Deubiquitinase, USP28 (ubiquitin specific peptidase 28), could maintain stability of proteins involved in tumor progression. This study was performed to investigate the role of USP28 in aerobic glycolysis of colorectal cancer. Our data showed that USP28 mRNA and protein expressions were enhanced in colorectal cancer tissues and cells. Functional assays demonstrated that overexpression of USP28 promoted cell proliferation and aerobic glycolysis of colorectal cancer, while USP28 inhibition could reverse these effects. Protein expression of Forkhead Box C1 (FOXC1) was increased by USP28 over-expression, whereas knockdown of USP28 aggravated cycloheximide (CHX; protein synthesis inhibitor) stimulated decrease of FOXC1. Moreover, proteasome inhibitor, MG132, could rescue USP28 silence-induced degradation of FOXC1. Overexpression of FOXC1 counteracted the suppressive effects of USP28 interference on colorectal cancer cell viability and aerobic glycolysis. In conclusion, USP28 enhanced cell viability and aerobic glycolysis of colorectal cancer by stabilizing FOXC1, suggesting that USP28-FOXC1 might be a novel therapeutic avenue for colorectal cancer.

scholarly journals Impact of HuR inhibition by the small molecule MS-444 on colorectal cancer cell tumorigenesis

Oncotarget ◽  
2016 ◽  
Vol 7 (45) ◽  
pp. 74043-74058 ◽  
Author(s):  
Fernando F. Blanco ◽  
Ranjan Preet ◽  
Andrea Aguado ◽  
Vikalp Vishwakarma ◽  
Laura E. Stevens ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
Small Molecule ◽  
Colorectal Cancer Cell

Dihydromyricetin reverses MRP2-induced multidrug resistance by preventing NF-κB-Nrf2 signaling in colorectal cancer cell

Phytomedicine ◽  
2020 ◽  
pp. 153414
Author(s):  
Ziyuan Wang ◽  
Xiaoting Sun ◽  
Yuanyuan Feng ◽  
Yang Wang ◽  
Lu Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Multidrug Resistance ◽  
Cancer Cell ◽  
Colorectal Cancer Cell

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.

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