RESUMEN
Fibroblast growth factor 9 (FGF9) is a member of the fibroblast growth factor family, which is widely expressed in the central nervous system (CNS). It has been reported that deletion of FGF9 leads to defects in cerebellum development, including Purkinje cell defect. However, it is not clear how FGF9 regulating cerebellar development remains to be determined. Our results showed that in addition to disrupt Bergmann fiber scaffold formation and granule neuron migration, deletion of neuronal FGF9 led to ataxia defects. It affected development and function of Purkinje cells, and also changed the action potential threshold and excitation frequency. Mechanistically, depletion of FGF9 significantly changed neurotransmitter contents in Purkinje cells and led to preferential increase in inflammation, even downregulation in ERK signaling. Together, the data demonstrate that neuronal FGF9 is required for the development and function of Purkinje cells in the cerebellum. Insufficient FGF9 during cerebellum development will cause ataxia defects.
RESUMEN
Objective: To explore the functional role of Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) in the progression of ovarian carcinoma (OC). Methods: RT-qPCR analysis and western blot were conducted to detect the mRNA and protein expression of CaMKK2, PI3K, PDK1 and Akt in OC tissues and cells, respectively. CCK-8 assay, transwell migration assay and flow cytometry were used to measure cell proliferation, migration and apoptosis, respectively. Results: CaMKK2, PI3K, PDK1 and Akt were highly expressed in OC tissues compared with the corresponding controls. CaMKK2 knockdown significantly suppressed the mRNA and protein expression of PI3K, PDK1 and Akt in HO8910 and OV90 cells. Moreover, CaMKK2 knockdown could dramatically repress cell proliferation, migration, and markedly elevate cell apoptosis in HO8910 and OV90 cells. Conclusions: CaMKK2 played a promotion role in OC progression via activating the PI3K/PDK1/Akt axis.
