This study investigated the effects of microRNA-135a (miR-135a) targeting of glycogen synthase kinase 3β (GSK3β) on the epithelial-mesenchymal transition (EMT), migration and invasion of bladder cancer (BC) cells by mediating the Wnt/β-catenin signaling pathway. BC and adjacent normal tissues were collected from 165 BC patients. Western blotting and quantitative real-time PCR were used to detect the expression of GSK3β, β-catenin, cyclinD1, E-cadherin, vimentin and miR-135a in BC tissues and cells. Cells were assigned to blank, negative control (NC), miR-135a mimics, miR-135a inhibitors, small interfering RNA (siRNA)-GSK3β or miR-135a inhibitors+siRNA-GSK3β groups. miR-135a, β-catenin, cyclinD1 and vimentin expression increased, while GSK3β and E-cadherin expression decreased in BC tissues compared with adjacent normal tissues. Compared with the blank and NC groups, the expression of miR-135a, β-catenin, cyclinD1 and vimentin was higher, and cell proliferation, migration, invasion and tumor growth were increased in the miR-135a mimics and siRNA-GSK3β groups. These groups showed an opposite trend in GSK3β and E-cadherin expression and cell apoptosis. The miR-135a inhibitors group was inversely correlated with the blank and NC groups. It was concluded that miR-135a accelerates the EMT, invasion and migration of BC cells by activating the Wnt/β-catenin signaling pathway through the downregulation of GSK3β expression.
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http://dx.doi.org/10.1038/emm.2017.239 | DOI Listing |
Pharmaceutics
December 2024
National Institute of Gastroenterology S. De Bellis, IRCCS Research Hospital, Via Turi 27, 70013 Castellana Grotte, BA, Italy.
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December 2024
Molecular Imaging and Therapy Research Unit, Department of Radiologic Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai 50200, Thailand.
Triple-negative breast cancer (TNBC) represents an aggressive form of breast cancer with few available therapeutic options. Chemotherapy, particularly with drugs like doxorubicin (DOX), remains the cornerstone of treatment for this challenging subtype. However, the clinical utility of DOX is hampered by adverse effects that escalate with higher doses and drug resistance, underscoring the need for alternative therapies.
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November 2024
Department of Biomedical Engineering, Chang Gung University, Taoyuan 33302, Taiwan.
This review explores the significant role of microfluidic technologies in advancing cancer research, focusing on the below key areas: droplet-based microfluidics, organ-on-chip systems, paper-based microfluidics, electrokinetic chips, and microfluidic chips for the study of immune response. Droplet-based microfluidics allows precise manipulation of cells and three-dimensional microtissues, enabling high-throughput experiments that reveal insights into cancer cell migration, invasion, and drug resistance. Organ-on-chip systems replicate human organs to assess drug efficacy and toxicity, particularly in the liver, heart, kidney, gut, lung, and brain.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Health Sciences Postgraduate Program, São Francisco University, Av. São Francisco de Assis, 218, Bragança Paulista, Sao Paulo 12916-900, Brazil.
The global increase in cancer cases and mortality has been associated with inflammatory processes, in which chemokines play crucial roles. These molecules, a subfamily of cytokines, are essential for the migration, adhesion, interaction, and positioning of immune cells throughout the body. Chemokines primarily originate in response to pathogenic stimuli and inflammatory cytokines.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Biomedical Sciences, Noorda College of Osteopathic Medicine, Provo, UT 84606, USA.
Besides various infectious and inflammatory complications, recent studies also indicated the significance of NLRP3 inflammasome in cancer progression and therapy. NLRP3-mediated immune response and pyroptosis could be helpful or harmful in the progression of cancer, and also depend on the nature of the tumor microenvironment. The activation of NLRP3 inflammasome could increase immune surveillance and the efficacy of immunotherapy.
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