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