ErbB signaling pathway； HIF-1 signaling pathway；Cell cycle； Melanoma；p53 signaling pathway；PI3K-Akt signaling pathway；Viral carcinogenesis；Hepatitis C；Hepatitis B；HTLV-I infection；Epstein-Barr virus infection；Chronic myeloid leukemia；Pathways in cancer；Proteoglycans in cancer；Transcriptional misregulation in cancer；Prostate cancer；Bladder cancer；Glioma

For instance, through its miRNA response elements (MREs) to compete for miR-106a-5p, lncRNA-FER1L4 regulates the expression of PTEN, RB1, RUNX1, VEGFA, CDKN1A, E2F1, HIPK3, IL-10, and PAK7.

Long noncoding RNA associated-competing endogenous RNAs in gastric cancer PTENP1 Functions as a Competing Endogenous RNA (ceRNA) to Regulate PTEN Expression by Sponging miR-499-5p.

ErbB signaling pathway；HIF-1 signaling pathway；Cell cycle；p53 signaling pathway；PI3K-Akt signaling pathway；Hepatitis C；Hepatitis B；Bladder cancer；Chronic myeloid leukemia；Melanoma；HTLV-I infection；Glioma；Epstein-Barr virus infection；Pathways in cancer；Transcriptional misregulation in cancer；Prostate cancer；Viral carcinogenesis；Proteoglycans in cancer

Mechanistically, we demonstrated that circ-ITCH up-regulates the expression of miR-17 and miR-224 target gene p21 and PTEN through 'sponging' miR-17 and miR-224, which suppressed the aggressive biological behaviors of BCa.

Circular RNA circ-ITCH inhibits bladder cancer progression by sponging miR-17/miR-224 and regulating p21, PTEN expression.

ErbB signaling pathway；HIF-1 signaling pathway；Cell cycle；p53 signaling pathway；PI3K-Akt signaling pathway；Hepatitis C；Hepatitis B；Bladder cancer；Chronic myeloid leukemia；Melanoma；HTLV-I infection；Glioma；Epstein-Barr virus infection；Pathways in cancer；Transcriptional misregulation in cancer；Prostate cancer；Viral carcinogenesis；Proteoglycans in cancer

circMTO1 suppresses HCC progression by acting as the sponge of oncogenic miR-9 to promote p21 expression, suggesting that circMTO1 is a potential target in HCC treatment.

circMTO1 suppresses HCC progression by acting as the sponge of oncogenic miR-9 to promote p21 expression, suggesting that circMTO1 is a potential target in HCC treatment.

Axon guidance；MAPK signaling pathway；Chemokine signaling pathway；Natural killer cell mediated cytotoxicity；Fc epsilon RI signaling pathway；B cell receptor signaling pathway；Phagosome；PI3K-Akt signaling pathway；Pancreatic cancer；Wnt signaling pathway；Leukocyte transendothelial migration；Amyotrophic lateral sclerosis (ALS)；VEGF signaling pathway；Regulation of actin cytoskeleton；Proteoglycans in cancer；Epithelial cell signaling in Helicobacter pylori infection；Osteoclast differentiation；Shigellosis；Focal adhesion；Adherens junction；Neurotrophin signaling pathway；Salmonella infection；Renal cell carcinoma；Viral myocarditis；Pancreatic secretion；Pathways in cancer；Colorectal cancer；Toll-like receptor signaling pathway；Fc gamma R-mediated phagocytosis；Bacterial invasion of epithelial cells；Viral carcinogenesis

Luciferase reporter assay indicated that MALAT1 and RAS-related C3 botulinum substrate 1 (Rac1) are targets of miR-101b. We uncovered that MALAT1 regulates Rac1 expression through miR-101b as a competing endogenous RNA (ceRNA), thereby influencing the proliferation, cell cycle and activation of primary HSCs.

MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis