Article Figures & Data
Figures
- 1
Mechanisms of oncogenesis. LTRs recruit transcription factors from the infected cell for retroviral gene transcription. These LTRs can also enhance transcription of the host cell genes, leading to uncontrolled tumor cell proliferation. Some HERVs encode potentially oncogenic proteins like Np9 and Rec that interact with transcription factors and activate immunosuppressor pathways, promoting oncogenesis. HERVs can also induce chromosomal translocations in somatic cells that could lead to tumor proliferation. HERVs also can promote an immunosuppressive response that may lead to cancer formation and spreading, because the Env protein has an immunosuppressive domain (ISD).
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Retranscription of HERVs would activate the innate response of sensors (pattern-recognition receptors or PRRs) of single RNA strand (RIG1 and MDA5) in cytosol of the cancer cells. This activates the signaling pathways leading to activation of TRAF family member-associated NF-κB activator (TANK)-binding kinase 1 (TBK1) that causes induction of the IFN-regulatory factor-3 and 7 (IRF-3 and IRF-7), NF-KB-dependent gene expression and subsequent production of IFN beta. This results in transcriptional activation of interferon stimulated genes with the production of cytokines, and increased expression of MHC type I on cancer cells.
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