Senescent cells secrete cytokines, chemokines and growth factors collectively known as the senescence-associated secretory phenotype (SASP) which can reinforce senescence and activate the immune response. However, it can also negatively impact neighbouring tissues facilitating tumor progression. We have previously shown that in proliferating cells the nuclear long non-coding RNA (lncRNA) MIR31HG inhibits p16/CDKN2A expression through interaction with polycomb repressor complexes (PRC1/2) and that during BRAF-induced senescence MIR31HG is overexpressed and translocates to the cytoplasm. Here, we show that MIR31HG regulates the expression of a subset of SASP components during BRAF-induced senescence. The SASP secreted from senescent cells depleted for MIR31HG fails to induce paracrine invasion without affecting the growth inhibitory effect. Mechanistically, MIR31HG interacts with YBX1 facilitating its phosphorylation at serine 102 (p-YBX1S102) by the kinase RSK. p-YBX1S102 induces IL1A translation which acts as upstream regulator inducing the transcription of the other SASP mRNAs. Our results suggest a dual role for MIR31HG in senescence depending on its cellular localization and points to the lncRNA as a potential therapeutic target in the treatment of senescence-related pathologies.