LncRNA H19 promotes tumor angiogenesis in smokers by targeting anti-angiogenic miRNAs

Abstract

A key concept in drug discovery is the identification of candidate therapeutic targets such as long noncoding RNAs (lncRNAs) because of their extensive involvement in neoplasms, and impressionability by smoking. Induced by exposure to cigarette smoke, lncRNA H19 targets and inactivates miR-29, miR-30a, miR-107, miR-140, miR-148b, miR-199a and miR-200, which control the rate of angiogenesis by inhibiting BiP, DLL4, FGF7, HIF1A, HIF1B, HIF2A, PDGFB, PDGFRA, VEGFA, VEGFB, VEGFC, VEGFR1, VEGFR2 and VEGFR3. Nevertheless, these miRNAs are often dysregulated in bladder cancer, breast cancer, colorectal cancer, glioma, gastric adenocarcinoma, hepatocellular carcinoma, meningioma, non-small-cell lung carcinoma, oral squamous cell carcinoma, ovarian cancer, prostate adenocarcinoma and renal cell carcinoma. As such, the present perspective article seeks to establish an evidence-based hypothetical model of how a smoking-related lncRNA known as H19 might aggravate angiogenesis by interfering with miRNAs that would otherwise regulate angiogenesis in a nonsmoking individual.