Metastamir-mediated immune evasion: MiR-10b downregulates the stress-induced molecule MICB, hence avoid recognition by NKG2D receptor

Pinchas Tsukerman; Jonatan Enk; Ofer Mandelboim

doi:10.4161/onci.22245

Metastamir-mediated immune evasion: MiR-10b downregulates the stress-induced molecule MICB, hence avoid recognition by NKG2D receptor

Pinchas Tsukerman, Jonatan Enk, Ofer Mandelboim^*

^*Corresponding author for this work

Department of Immunology and Cancer Research

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

Metastases are responsible for more than 90% of cancer-related deaths. We have recently reported that miR-10b inhibits the expression of MICB, a stress-induced ligand of the activating natural killer (NK)-cell receptor NKG2D. Here, we discuss our findings, which link metastasis formation to immune evasion.

Original language	English
Article number	e22245
Journal	OncoImmunology
Volume	2
Issue number	1
DOIs	https://doi.org/10.4161/onci.22245
State	Published - Jan 2013

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abstract = "Metastases are responsible for more than 90% of cancer-related deaths. We have recently reported that miR-10b inhibits the expression of MICB, a stress-induced ligand of the activating natural killer (NK)-cell receptor NKG2D. Here, we discuss our findings, which link metastasis formation to immune evasion.",

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AB - Metastases are responsible for more than 90% of cancer-related deaths. We have recently reported that miR-10b inhibits the expression of MICB, a stress-induced ligand of the activating natural killer (NK)-cell receptor NKG2D. Here, we discuss our findings, which link metastasis formation to immune evasion.

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Metastamir-mediated immune evasion: MiR-10b downregulates the stress-induced molecule MICB, hence avoid recognition by NKG2D receptor

Abstract

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