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. 2021 Jun 12;23(10):1647–1655. doi: 10.1093/neuonc/noab142

Table 2.

Potential Linkages of HERVs as Cancer-Promoting Agents in Glioma

Study HERV-element Mechanism Cancer Cellular Gene Gene Role in Glioma
18 Rec/Np9 Activation of C-MYC oncogene PLZF Upregulated three-fold in glioma samples
21 Np9 Amplifying Notch signaling via LNX degradation LNX Downregulated in gliomas
28 HERV-K Gene inactivation by insertional mutagenesis BRCA2 Germline inactivation mutations noted in some samples
28 HERV-K Gene inactivation by insertional mutagenesis XRCC1 Polymorphisms associated with increased risk of gliomas
32 HERV-K LTR Chromosomal rearrangement activating ETV1 proto-oncogene ETV1 ETV1 overexpression associated with aggressive phenotype in oligodendrogliomas
33 HERV LTR Chromosomal rearrangement PMS2 Association with CMMRD
37 HERV LTR cis activation of promoter CSF1R Implicated in Glioma invasion41
40 HERV LTR cis activation of promoter ERBB4 Associated with aggressive glioma phenotype42
43 HERV-K Correlation to CD133+ stem-cell markers in melanoma CD133 Glioma stem-cell marker, associated with aggressive phenotype
8 HERV-K (Hml-2) Maintenance of stemness through interactions with CD98HC/mTOR CD98HC CD98 upregulated in astrocytic tumors, facilitates tumor proliferation, amino acid transport44

Abbreviations: CSF1R, colony-stimulating factor 1 receptor; ERBB4, receptor tyrosine-protein kinase; ETV1, ETS translocation variant 1; LNX, E3 ubiquitin-protein ligase; PLZF, promyelocytic leukemia zinc finger protein; PMS2, Mismatch repair endonuclease; XRCC1, X-ray repair cross-complementing protein 1.