HOTAIR Up-Regulation Activates NF-κB to Induce Immunoescape in Gliomas.

ABSTRACT:

Background

Checkpoint blockade therapies targeting programmed death ligand 1 (PD-L1) and its receptor programmed cell death 1 promote T cell-mediated immune surveillance against tumors and have been associated with significant clinical benefit in cancer patients. The long-stranded non-coding RNA HOTAIR is highly expressed and associated with metastasis in a variety of cancer types and promotes tumor metastasis at least in part through association with the PRC2 complex that induces redirection to hundreds of genes involved in tumor metastasis. Here, we report that HOTAIR is an activator lncRNA of the NF-κB pathway and demonstrate that its apparent upregulation promotes inflammatory signaling and immune escape in glioma cells.

Methods

Bioinformatics analysis was used to elucid

SUBMITTER: Wang Y 

PROVIDER: S-EPMC8649724 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature