Abstract
CAPON is an adapter protein for nitric oxide synthase 1 (NOS1). CAPON has two isoforms in the human brain: CAPON-L (long form of CAPON) and CAPON-S (short form of CAPON). Recent studies have indicated the involvement of CAPON in tumorigenesis beyond its classical role in NOS1 activity regulation. In this study, we found that the protein levels of CAPON-S, but not than CAPON-L, were significantly decreased in glioma tissues. Therefore, we established lentivirus-mediated stable cell lines with CAPON-S overexpression or down-regulation, and investigated the role of CAPON-S in the proliferation of glioma cells by using CCK8, EdU, and flow cytometry assays. Overexpression of CAPON-S reduced the cell variability and the percentage of EdU-positive cells, and arrested the cells in the G1 phase in glioma cells. Silencing of CAPON by short-hairpin RNA showed the opposite effects. Furthermore, an intracellular signaling array revealed that overexpression of CAPON-S resulted in a remarkable reduction in the phosphorylation of Akt and S6 ribosomal protein in glioma cells, which was further confirmed by Western blot. These findings suggest that CAPON may function as a tumor suppressor in human brain glioma and that the inactivation of the Akt signaling pathway caused by CAPON-S overexpression may provide insight into the underlying mechanism of CAPON in glioma cell proliferation.
Highlights
Glioma is the most common and aggressive tumor in the central nervous system [1]
Further functional experiments of stable overexpression or down-regulation demonstrated that CAPON had an inhibitory effect on the proliferation of glioma cells
These findings indicate that CAPON may serve as a tumor suppressor in glioma, possibly through inactivating the Akt signaling pathway
Summary
Glioma is the most common and aggressive tumor in the central nervous system [1]. It is characterized by uncontrolled proliferation, anti-apoptotic effect, invasion, and migration [2]. NO is produced from arginine predominantly by. 2 of 11 2 of 11 arginine predominantly by nitric oxide synthase 1 [10]. IItt wwaass pprreevviioouussllyy rreeppoorrtteedd tthhaatt CCAAPPOONN wwaass llooccaatteedd iinn tthhee ccyyttooppllaassmm ooff ccuullttuurreedd rraatt pprriimmaarryy aassttrrooccyytteess [[2233]]. InInthtihsisstusdtuyd, yw, ewfeirsfitrlystalyssaesssseesdsethdetehxeperexspsrieosnsicohnancgheasnogfesCAofPCOANP(OinNclu(dininclgudbointhg CboAthPOCNA-PLOaNn-dL aCnAdPCOANP-SO)Ni-nS)hiunmhaunmagnliogmliaomtiasstuisessueasnadndnonnotnutmumororbrbarianintitsissusueess aanndd tthheenn iinnvveessttiiggaatteedd tthhee rroollee ooff CCAAPPOONN iinn tthhee pprroolliiffeerraattiioonn ooff gglliioommaa cceellllss. IInn aaddddiittiioonn,, wwee ssccrreeeenneedd tthhee CCAAPPOONN--SS–-oovveerreexxpprreessssiinngg gglliioommaa cceellllss ttoo rreevveeaall tthhee cchhaannggeess iinn ssoommee iimmppoorrttaanntt ssiiggnnaalliinngg ppaatthhwwaayyss rreellaatteedd ttoo ttuummoorriiggeenneessiiss
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