The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype

Abstract Oncogene-induced senescence provides a barrier against malignant transformation. However, it can also promote cancer through the secretion of plethora factors released by senescent cells, called associated secretory phenotype (SASP). We have previously shown that in proliferating nuclear lncRNA MIR31HG inhibits p16/CDKN2A expression interaction with polycomb repressor complexes and during BRAF-induced senescence, is overexpressed translocates to cytoplasm. Here, we show regulates subset SASP components senescence. The secreted from cells depleted for fails induce paracrine invasion without affecting growth inhibitory effect. Mechanistically, interacts YBX1 facilitating its phosphorylation at serine 102 (p-YBX1 S102 ) kinase RSK. p-YBX1 induces IL1A translation which activates transcription other mRNAs. Our results suggest dual role depending on localization points as potential therapeutic target treatment senescence-related pathologies.