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https://www.selleckchem.com/products/muvalaplin.html miR-584-5p and miR-34a-5p in si-LINC0196-NC, miR-584-5p-NC, and miR-34a-5p-NC groups decreased significantly (P less then 0.05). The proliferation rate, migration rate, and invasiveness of SK-N-SH cells in miR-584-5p and miR-34a-5p groups were lower than those in si-LINC0196-NC, miR-584-5p-NC, and miR-34a-5p-NC groups, while the apoptosis rate increased (P less then 0.05). After miR-584-5p and miR-34a-5p transfections, the relative activities of WT-LINC0196 and WT-TRIM59 dual luciferase were greatly inhibited (P less then 0.05). LINC0196 could regulate TRIM59 by regulating miR-584-5p and miR-34a-5p, thereby indirectly regulating cell proliferation, apoptosis, migration, and invasion of SK-N-SH cells.To investigate the effect of the FGFR2-CCDC6 fusion gene on cell proliferation and its mechanism of action, pCDNA3.1- FGFR2bWT, pCDNA3.1- FGFR2-CCDC6 expression plasmids were transiently transfected into Hucct-1 cells using Lipo-2000 liposomes. The effect of the fusion gene on cell proliferation was examined by MTT and the expression of FGFR2/AKT/signaling pathway proteins was detected by Western blot. Results showed that Hucct-1 cells transfected with the FGFR2-CCDC6 fusion gene showed increased FGFR2 protein expression (P less then 0.001) and significantly higher cell proliferation capacity (P less then 0.001) compared to normal controls. It was concluded that The FGFR2-CCDC6 fusion gene excessively activates the AKT, and ERK signaling pathway downstream of FGFR2 and plays a role in promoting cell proliferation.Acute myelogenous leukemia (AML) is a very common hematopoietic malignancy. Hematopoietic stem cell transplantation can improve the therapeutic effect of AML, but the 5-year survival rate is very low. CD123 imbalance, abnormal gene expression, and epigenetics play an important role in the pathogenesis of AML. This research was to explore the differential expression of CD123-related long non-coding RNA (lncRNA)
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