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The role of CD44 in the naked-mole rat oligodendrocyte progenitor cells

ABSTRACT: The role of CD44 in naked-mole rats (NMR) oligodendrocyte progenitor cells (OPCs) were evaluated by comparing the transcriptome of control and CD44-knockdown NMR OPCs.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Heterocephalus glaber

SUBMITTER: Masaki Takasugi

PROVIDER: E-MTAB-9166 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Transcriptome of long-lived naked-mole rat (NMR) oligodendrocyte progenitor cells (OPCs) were compared with OPCs of other species.

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The role of CD44 in the naked-mole rat oligodendrocyte progenitor cells

Project description:The role of CD44 in the naked-mole rat oligodendrocyte progenitor cells

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Transformation of Naked Mole-Rat Cells

Project description:The naked mole-rat (NMR), Heterocephalus glaber, is a mouse-sized subterranean rodent native to East Africa. Research on NMRs is intensifying in an effort to gain leverage from their unusual physiology, long-life span and cancer resistance for the development of new theraputics. Few studies have attempted to explain the reasons behind the NMR’s cancer resistance, but most prominently Tian et al. reported that NMR cells produce high-molecular weight hyaluronan as a potential cause for the NMR’s cancer resistance. Tian et al. have shown that NMR cells are resistant to transformation by SV40 Large T Antigen (SV40LT) and oncogenic HRAS (HRASG12V), a combination of oncogenes sufficient to transform mouse and rat fibroblasts. We have developed a number of lentiviral vectors to deliver both these oncogenes and generated 106 different cell lines from five different tissues and eleven different NMRs, and report here that contrary to Tian et al.’s observation, NMR cells are susceptible to oncogenic transformation by SV40LT and HRASG12V. Our data thus point to a non-cell autonomous mechanism underlying the remarkable cancer resistance of NMRs. Identifying these non-cell autonomous mechanisms could have significant implications on our understanding of human cancer development.

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