Long non-coding RNA PACER

Recent investigations into PACER’s role as an inflammatory regulator and our expertise in AA signaling have prompted our examination of how PACER affects COX-2 expression in lung cancer [16]. Our recent publication identifies a strong correlation between PACER and COX-2 expression in lung adenocarcinoma patient samples using bioinformatic tools. Additionally, our siRNA-mediated knockdown of PACER demonstrates a direct relationship between PACER and COX-2 expression in lung cancer cells.

While previous studies have used lipopolysaccharide (LPS) to elicit an immune response, we demonstrate that physiologically relevant cytokines increase both PACER and COX-2 expression in LUAD cell lines. We provide evidence of potential regulatory feedback mechanisms involving PGE2. Furthermore, we identify the possibility of additional mechanisms regulating PACER transcription by interrogating the COX-2 transcription factors (TFs) AP-1 and NF-ϰB. Our results demonstrate a clear relationship between PACER expression and the transcriptional regulation of COX-2 in lung cancer cell lines. Based on the literature and our previous studies we hypothesize that Inhibition of PACER expression decreases lung cancer cell proliferation and migration and has key regulatory effects on the arachidonic acid metabolic pathway and beyond.