Biallelic loss of FAM46C triggers tumor growth with concomitant activation of Akt signaling in multiple myeloma cells.

ABSTRACT: Loss of heterozygosity or mutation of the family with sequence similarity 46, member C (FAM46C) gene on chromosome band 1p12 is associated with shorter overall survival of patients with multiple myeloma (MM). In this study, using human MM cell lines (KMS-11, OCI-My5, and ANBL-6), we generated FAM46C^-/- cell clones and examined the effect of disruption of FAM46C on cell survival and cellular signaling. Cell proliferation assays showed increased clonogenicity of FAM46C^-/- KMS-11 cells compared to WT cells. Xenograft experiments showed significantly shorter overall survival of mice harboring the FAM46C^-/- cell-derived tumors than mice with the FAM46C^WT cell-derived tumors. Notably, levels of phosphorylated Akt and its substrates increased both in vi

SUBMITTER: Kanasugi J 

PROVIDER: S-EPMC7226186 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature