The pioneering work from Chen’s lab identified Siglec-15 as novel tumor immune suppressor, while the regulatory mechanisms underlying the broad up-regulation of Siglec-15 in human cancers were obscure currently. Here we found long non-coding RNA (lncRNA) LINC00973 was higher in Siglec-15-positive clear-cell renal cell carcinoma (ccRCC), and LINC00973 positively regulated Siglec-15 expression at transcriptional level. This effect was evidently dependent on miR-7109-3p (designated as miR-7109 hereafter), and we provided evidences supporting that Siglec-15 as direct target of miR-7109. Via sponging miR-7109, LINC00973 functioned as competing endogenous RNA (ceRNA) to control cell surface abundance of Siglec-15, and consequently was involved in cancer immune suppression. We further demonstrated that LINC00973 and miR-7109 expression in ccRCC antagonistically influenced immune activation of co-cultured Jurkat cells. Our study highlighted the importance of LINC00973-miR-7109-Siglec-15 in immune evasion in ccRCC, which offered significant opportunity for both therapeutic intervention and diagnostic/prognostic exploitations.This article is protected by copyright. All rights reserved.
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