This correspondence concerns a recent publication inCancer Cellby Liu et al.1 who analyzed a long noncoding RNA (lncRNA) that they designated “NKILA”. Liu et al. found thatNKILA(1) is upregulated by immunostimulants, (2) has a promoter with an NF-ĸB binding motif, (3) can bind to the p65 protein of the NF-ĸB transcription factor and then interfere with phosphorylation of IĸBα, and (4) negatively affects functions that involve NF-ĸB pathways. And, importantly, they found that (5) lowNKILAexpression in breast cancers is associated with poor patient prognosis. However, they entirely failed to mentionPMEPA1, a gene which runs antisense toNKILA, and the expression of which is associated with several tumors and which encodes a protein that participates in immune pathways.ThePMEPA1locus, including its promoter region, which Liu et al.1only discuss in regard toNKILA, is highly conserved through evolution. Our impression is thatNKILAemerged only later in evolution, possibly as an additional means ofPMEPA1regulation. Liu et al., however, only consider direct binding betweenNKILAand NF-ĸB as the mechanism for theirin vivoobservations ofNKILAfunction, but do not provide solid evidence for their model. Ifin vivoobservations by Liu et al. could be explained byNKILAregulation ofPMEPA1, it would contribute to the establishment ofPMEPA1as an important topic of cancer research. We feel that the herein presented discussion is necessary for a correct interpretation of the Liu et al. article.
ESR1-Stabilizing Long Noncoding RNA TMPO-AS1 Promotes Hormone-Refractory Breast Cancer Progression
