In ovarian cancer, NF-κB transcriptionally upregulates HOTAIR expression during cisplatin-induced DNA damage, and HOTAIR facilitates degradation of the NF-κB inhibitor IκBα and thus enhances NF-κB activation, thereby creating a feed-forward regulatory circuit between NF-κB and HOTAIR [25]. Here, NFKB1 is linked to ovarian carcinoma.