Objective: To investigate the suppression effect of exogenous fragile histidine triad (FHIT) gene on biological property of MEC-1 cells.
Methods: In order to study the FHIT function in MEC-1 cells, wild-type FHIT gene was transferred into mucoepidermoid carcinoma MEC-1 cells. The proliferation and kinetics, cell cycle, clonal forming rate, and apoptosis of MEC-1 cells, before and after FHIT gene transfection in vitro, and tumor loci formed on mice after injection of transferred MEC-1 cells in vivo were observed by immunochemical staining, flow cytometry analysis, and so on.
Results: It can be seen that exogenous FHIT gene transfer could significantly inhibit the proliferation and reduce the kinetics of MEC-1 cells in vitro, prolong DT from (21.03+/-0.41) h to (26.86+/-0.71) h, and also keep less cells in cell cycle phase S, whilst more cells in phase G1, Additionally, the exogenous FHIT was found to be able to remarkably suppress MEC-1 cells of forming tumor loci in nude mice by lessen tumor weight, and promote higher differentiation of MEC-1 cells to be mucous cells.
Conclusion: Exogenous FHIT gene could suppress the proliferation, tumorigenicity and improve the differentiation of MEC-1 cells, in vitro and in vivo.
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Arch Med Res
November 2024
Institute of Pathological Physiology, First Faculty of Medicine, Charles University, Prague, Czech Republic. Electronic address:
Background: Cell cycle progression and leukemia development are tightly regulated processes in which even a small imbalance in the expression of cell cycle regulatory molecules and microRNAs (miRNAs) can lead to an increased risk of cancer/leukemia development. Here, we focus on the study of a ubiquitous, multifunctional, and oncogenic miRNA-hsa-miR-155-5p (miR-155, MIR155HG), which is overexpressed in malignancies including chronic lymphocytic leukemia (CLL). Nonetheless, the precise mechanism of how miR-155 regulates the cell cycle in leukemic cells remains the subject of extensive research.
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December 2024
Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), PO Box 70250, Ciudad de México 04510, Mexico. Electronic address:
Mecamylamine, a noncompetitive blocker of nicotinic acetylcholine receptors (nAChRs), is the racemic mixture of two stereoisomers: S-(+)-mecamylamine (S-mec) and R-(-)-mecamylamine (R-mec), with distinct interactions with α4β2 nAChRs. It has been shown that mecamylamine increases glutamate release and excites serotonergic (5-HT) neurons in the dorsal raphe nucleus (DRN). In this study, we separately evaluated the effects of S-mec and R-mec on 5-HT neuron excitability.
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September 2024
Department of Systems Biology, Beckman Research Institute, City of Hope National Comprehensive Cancer Center, Monrovia, California.
Cancer Cell Int
July 2024
Institute of Pathological Physiology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Hypoxia represents one of the key factors that stimulates the growth of leukemic cells in their niche. Leukemic cells in hypoxic conditions are forced to reprogram their original transcriptome, miRNome, and metabolome. How the coupling of microRNAs (miRNAs)/mRNAs helps to maintain or progress the leukemic status is still not fully described.
View Article and Find Full Text PDFLeuk Res
September 2024
Department of Hematology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang 330006, China. Electronic address:
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