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The innate immune receptors, such as toll‐like receptor 3 ( TLR 3), melanoma differentiation‐associated 5 ( MDA 5) and retinoic acid‐inducible gene‐I ( RIG ‐I), have been shown to be differentially expressed in neuroblastoma ( NB ) and promote ds RNA  poly (I:C)‐induced  NB  suppression in vitro and in vivo. However, the role of another important innate immune cytosolic sensor, laboratory of genetics and physiology 2 ( LGP 2), in the cancer behavior of  NB  remains unclear. Here, we demonstrated that the expression levels of  LGP 2 were either low or undetectable in all  NB  cell lines tested with or without   MYCN   amplification.  LGP 2 expression levels were significantly increased only in  NB  cells without   MYCN   amplification, including  SK ‐N‐ AS  and  SK ‐N‐ FI  after poly (I:C) treatment in vitro and in mouse xenograft models. Ectopic expression of  LGP 2 in  NB  cells significantly enhanced poly (I:C)‐induced  NB  cell death associated with downregulation of  MDA 5,  RIG ‐I,  MAVS  and Bcl‐2, as well as upregulation of Noxa and  tB id. By immunofluorescence analyses,  LGP 2 localized mainly in the cytoplasm of  NB  cells after poly (I:C) treatment. In human  NB  tissue samples, cytoplasmic  LGP 2 expression was positively correlated with histological differentiation and inversely correlated with   MYCN   amplification. Positive cytoplasmic  LGP 2 expression in tumor tissues could predict a favorable outcome in  NB  patients independent of other prognostic factors. In short,  LGP 2 was effective in promoting poly (I:C)‐induced  NB  suppression and cytoplasmic  LGP 2 can serve as an independent favorable prognostic factor in  NB  patients.

Innate immune sensor laboratory of genetics and physiology 2 suppresses tumor cell growth and functions as a prognostic marker in neuroblastoma