We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion.

LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma

mTOR signaling pathway；HIF-1 signaling pathway；Hypertrophic cardiomyopathy (HCM)；Glioma；Prostate cancer；Oocyte meiosis；p53 signaling pathway；PI3K-Akt signaling pathway；Proteoglycans in cancer；Melanoma；Focal adhesion；Long-term depression；Transcriptional misregulation in cancer；Ovarian steroidogenesis；Progesterone-mediated oocyte maturation；Aldosterone-regulated sodium reabsorption；Pathways in cancer；Dilated cardiomyopathy

Furthermore, we identified MHENCR as a competitively endogenous RNA, which specifically bound to miR-425 and miR-489, upregulated their target genes IGF1 and SPIN1 expression, and further activated PI3K-Akt pathway.

Long noncoding RNA MHENCR promotes melanoma progression via regulating miR-425/489-mediated PI3K-Akt pathway

Axon guidance；Phagosome；PI3K-Akt signaling pathway；Focal adhesion；ECM-receptor interaction；Toxoplasmosis；Cell adhesion molecules (CAMs)；Leukocyte transendothelial migration；Regulation of actin cytoskeleton；Hypertrophic cardiomyopathy (HCM)；Dilated cardiomyopathy；Proteoglycans in cancer；Arrhythmogenic right ventricular cardiomyopathy (ARVC)；Bacterial invasion of epithelial cells；Leishmaniasis；Pathogenic Escherichia coli infection；Pertussis；Pathways in cancer；Small cell lung cancer；Shigellosis

We further found that the expression and function of miR-183 were suppressed by MALAT1. Integrin β1 (ITGB1) was then speculated and confirmed as a direct target of miR-183. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1.

Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation

Furthermore, we identified MHENCR as a competitively endogenous RNA, which specifically bound to miR-425 and miR-489, upregulated their target genes IGF1 and SPIN1 expression, and further activated PI3K-Akt pathway.

Long noncoding RNA MHENCR promotes melanoma progression via regulating miR-425/489-mediated PI3K-Akt pathway