Lung cancer is the most common solid tumor and the leading cause of cancer-related mortality worldwide. miR-21 is one of the most commonly observed aberrant miRNAs in human cancers. However, the biological roles of miR-21 in glucose metabolism of non-small cell lung cancer (NSCLC) cells remain unknown. In the present study, our findings demonstrated that miR-21 promoted glucose uptake and increased TXNIP expression. miR-21 increased lactate generation and decreased oxygen consumption in NSCLC cells. Moreover, we found that miR-21 promoted glycolysis and decreased OXPHOS. Mechanistically, fructose-1,6-biphosphatase (FBP1) was a direct target of miR-21 and observed a negative correlation between miR-21 and FBP1 in NSCLC samples. Restoring FBP1 expression reversed the effects induced by miR-21 overexpression in NSCLC cells. Together, our findings suggest the critical role of miR-21 in glucose metabolism through suppression of FBP1 in NSCLC cells. miR-21 may be a potential target of NSCLC treatment.
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Mol Cancer
January 2025
Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, via Campi, 287, Modena, 41125, Italy.
B cells have emerged as central players in the tumor microenvironment (TME) of non-small cell lung cancer (NSCLC). However, although there is clear evidence for their involvement in cancer immunity, scanty data exist on the characterization of B cell phenotypes, bioenergetic profiles and possible interactions with T cells in the context of NSCLC. In this study, using polychromatic flow cytometry, mass cytometry, and spatial transcriptomics we explored the intricate landscape of B cell phenotypes, bioenergetics, and their interaction with T cells in NSCLC.
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January 2025
Department of Pathology, The Second Xiangya Hospital of Central South University, Changsha, China.
MicroRNA (miRNA) dysregulation has been identified in several carcinomas, including non-small cell lung cancer (NSCLC), and is known to play a role in the development and progression of this disease. We initially conducted a miRNA microarray analysis, which revealed that the MNK inhibitor CGP57380 increased the expression of miR-150-3p. A similar analysis was performed using data from The Cancer Genome Atlas (TCGA).
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School of Pharmacy, Faculty of Medicine & State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
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January 2025
State Key Laboratory of Molecular Oncology, CAMS Key Laboratory of Translational Research on Lung Cancer, Department of Medical Oncology, National Cancer Centre/National Clinical Research Centre for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences Peking Union Medical College, Beijing, 100021, China. Electronic address:
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