SNORD35A: SNORD35A has been shown to potentiate the oncogenic effects of the AML1-ETO fusion in leukemia through rRNA methylation [PMC6294694]. SNORD35A binding is increased on the 3′ splice site, snoU2-30 binding is enriched in the 5′ splice site, and SNORD38A shows an enrichment on the polypyrimidine tract [PMC9226514]. SNORD26 and SNORD96A are involved in determining the chondrocyte phenotype [PMC8638817]. Knockout of SNORD34, SNORD35A, and SNORD43 impaired clonogenic growth in a cell model, and depletion of SNORD14D reduced colony formation without affecting 18S-C762 methylation [PMC7114786]. Deletion of SNORD14D or SNORD35A suppresses clonogenic potential of leukemia cells in vitro and delays leukemogenesis in vivo [PMC7114786]. Knockdown of SNORD14D or SNORD35A also suppresses clonogenic potential of leukemia cells in vitro and delays leukemogenesis in vivo [PMC6629867]. Increased levels of three box C/D snoRNAs, including SNORD35A, were seen when CHO cells were exposed to fatty acids [PMC6466398]. RPL13A is a host gene encoding several snoRNAs including SNOD32a, SNOD33, and SNOD35a, and deregulation of these snoRNAs are associated with different types of cancer [PMC6466398]. Among other genes, downregulation of SNOD34, SNOD35A, SNOD38B, and SNOD71A was observed when expression of HOXA10 was silenced leading to impaired homologous recombination pathway and diminished temozolomide resistance [PMC5747948].