<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334395/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species> Mus musculus</species><species>Heterocephalus glaber</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334395</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptional profiling of epidermal keratinocytes from Naked mole-rats and mice</name><description>We compared expressions of cancer-related genes (tumor suppressor genes and oncogenes) between homeostatic epidermal keratinocytes from Naked mole-rats and FVB mice. Bulk RNA-seq analyses revealed that homeostatic epidermal keratinocytes in Naked mole-rats maintain high expression of tumor suppressor genes that inhibit cell proliferation and activity of pro-oncogenic Wnt, IGF and Hedgehog signaling pathways, stimulate apoptosis and DNA repair, which is associated with downregulation of several key oncogenes stimulating skin carcinogenesis. In contrast to Naked mole-rats, mouse keratinocytes predominantly express tumor suppressor genes linked to cell adhesion, growth factors signaling, nuclear receptors and transcriptional regulators, as well as show decreased expression of oncogenes driving carcinogenesis outside of the skin.</description><dates><publication>2026/07/09</publication></dates><accession>GSE334395</accession><cross_references><GSM>GSM9787407</GSM><GSM>GSM9787406</GSM><GSM>GSM9787409</GSM><GSM>GSM9787408</GSM><GSM>GSM9787405</GSM><GSM>GSM9787404</GSM><GPL>17021</GPL><GPL>21195</GPL><GSE>334395</GSE><taxon> Mus musculus</taxon><taxon>Heterocephalus glaber</taxon></cross_references></HashMap>