The secret identities of TMPRSS2: Fertility factor, virus trafficker, inflammation moderator, prostate protector and tumor suppressor
نویسندگان
چکیده
The human TMPRSS2 gene is pathogenetically implicated in both coronaviral lung infection and prostate cancer, suggesting its potential as a drug target contexts. SARS-COV-2 spike polypeptides are primed by the host transmembrane protease, triggering virus fusion with epithelial cell membranes followed an endocytotic internalisation process that bypasses normal endosomal activation of cathepsin-mediated innate immunity; viral co-opting thus favors microbial survivability attenuating inflammatory responses. In contrast, most early hormone-dependent cancers express TMPRSS2:ERG genes arising from deletions eliminate coding region while juxtaposing androgen-inducible promoter open reading frame ERG, upregulating pro-inflammatory ERG functionally disabling TMPRSS2. Moreover, oxidative DNA damage selects for TMPRSS2:ERG-fused cancers, whereas patients treated antiinflammatory drugs develop fewer these fusion-dependent tumors. These findings imply protects enabling bypass pathogens which could otherwise trigger inflammation-induced predisposes to fusions. Hence, high oncogenic selectability fusions may reflect unique synergy between androgenic gain-of-function fusogenic loss-of-function, cautioning against use TMPRSS2-inhibitory prevent or treat cancer.
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ژورنال
عنوان ژورنال: Tumor Biology
سال: 2021
ISSN: ['1423-0380', '1010-4283']
DOI: https://doi.org/10.3233/tub-211502