Apoptosis；MAPK signaling pathway；Acute myeloid leukemia；ErbB signaling pathway；Chemokine signaling pathway；Fc gamma R-mediated phagocytosis；Insulin signaling pathway；Pathways in cancer；Melanoma；Dopaminergic synapse；Colorectal cancer；Estrogen signaling pathway；HTLV-I infection；Toll-like receptor signaling pathway；Glioma；Adipocytokine signaling pathway；HIF-1 signaling pathway；Jak-STAT signaling pathway；Proteoglycans in cancer；Toxoplasmosis；B cell receptor signaling pathway；Small cell lung cancer；Progesterone-mediated oocyte maturation；Non-small cell lung cancer；Measles；Fc epsilon RI signaling pathway；mTOR signaling pathway；PI3K-Akt signaling pathway；Chagas disease (American trypanosomiasis)；Hepatitis C；VEGF signaling pathway；Prostate cancer；Renal cell carcinoma；Tuberculosis；Influenza A；T cell receptor signaling pathway；Osteoclast differentiation；Carbohydrate digestion and absorption； Endometrial cancer；Pancreatic cancer；Chronic myeloid leukemia；Cholinergic synapse；Hepatitis B；Focal adhesion；Epstein-Barr virus infection； Neurotrophin signaling pathway；Tight junction

Moreover, SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-β-activated kinase 1 (TAK1).

The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma

Regulation of autophagy；mTOR signaling pathway

We further explored the molecular mechanisms by which Malat1 exerted regulatory effects, and found that Malat1 served as an endogenous sponge to downregulate miR-26b expression by binding directly to miR-26b. Furthermore, Malat1 overturned the inhibitory effect of miR-26b on BMEC autophagy and survival, which involved in promoting the expression of miR-26b target ULK2.

Long noncoding RNA Malat1 is a potent autophagy inducer protecting brain microvascular endothelial cells against oxygen-glucose deprivation/reoxygenation-induced injury by sponging miR-26b and upregulating ULK2 expression.