MYC can promote nucleolar rRNA transcription by directly activating Pol I-mediated transcription of ribosomal genes, as well as by upregulating Pol II-mediated transcription of “Pol I regulon” genes. Concomitantly, MYC can also promote mitoribosome synthesis by upregulating Pol II-mediated transcription of genes encoding factors necessary for mitochondrial rRNA transcription (POLRMT and TFAM) and mitochondrial ribosomal proteins (PTCD3, MRPS5, and MRPS27). Drugs inhibiting Pol I (e.g. CX-5461), mitochondrial rRNA transcription (e.g. 2’-C-MeA), or mitoribosome function (e.g. doxycycline) could be used, alone or in combination, to target MYC-overexpressing cancer cells, such as ovarian cancer cells.