Natural killer cell mediated cytotoxicity；MAPK signaling pathway；ErbB signaling pathway；Chemokine signaling pathway；PI3K-Akt signaling pathway；Insulin signaling pathway；Hepatitis C；Long-term potentiation；Progesterone-mediated oocyte maturation；Dorso-ventral axis formation；Axon guidance；Endometrial cancer；Regulation of actin cytoskeleton；VEGF signaling pathway；Long-term depression；Estrogen signaling pathway；Cholinergic synapse；Melanogenesis；Hepatitis B；Viral carcinogenesis；Tight junction；Neurotrophin signaling pathway；GnRH signaling pathway；Gap junction；Glioma；T cell receptor signaling pathway； Alcoholism；Prostate cancer；Serotonergic synapse；Bladder cancer；Non-small cell lung cancer；Chronic myeloid leukemia；HTLV-I infection；B cell receptor signaling pathway；Pathways in cancer；Aldosterone-regulated sodium reabsorption；Colorectal cancer；Melanoma；Acute myeloid leukemia；Proteoglycans in cancer；Pancreatic cancer；Renal cell carcinoma；Thyroid cancer；Fc epsilon RI signaling pathway

We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect. Conversely, Malat1 knockdown inhibits proliferation and invasion by GBC cells while increasing apoptosis.

Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206

Natural killer cell mediated cytotoxicity；MAPK signaling pathway；ErbB signaling pathway；Chemokine signaling pathway；PI3K-Akt signaling pathway；Insulin signaling pathway；Hepatitis C；Long-term potentiation；Progesterone-mediated oocyte maturation；Dorso-ventral axis formation；Axon guidance；Endometrial cancer；Regulation of actin cytoskeleton；VEGF signaling pathway；Long-term depression；Estrogen signaling pathway；Cholinergic synapse；Melanogenesis；Hepatitis B；Viral carcinogenesis；Tight junction；Neurotrophin signaling pathway；GnRH signaling pathway；Gap junction；Glioma；T cell receptor signaling pathway； Alcoholism；Prostate cancer；Serotonergic synapse；Bladder cancer；Non-small cell lung cancer；Chronic myeloid leukemia；HTLV-I infection；B cell receptor signaling pathway；Pathways in cancer；Aldosterone-regulated sodium reabsorption；Colorectal cancer；Melanoma；Acute myeloid leukemia；Proteoglycans in cancer；Pancreatic cancer；Renal cell carcinoma；Thyroid cancer；Fc epsilon RI signaling pathway

In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration.

LncRNA-RMRP Acts as an Oncogene in Lung Cancer

Natural killer cell mediated cytotoxicity；MAPK signaling pathway；ErbB signaling pathway；Chemokine signaling pathway；PI3K-Akt signaling pathway；Insulin signaling pathway；Hepatitis C；Long-term potentiation；Progesterone-mediated oocyte maturation；Dorso-ventral axis formation；Axon guidance；Endometrial cancer；Regulation of actin cytoskeleton；VEGF signaling pathway；Long-term depression；Estrogen signaling pathway；Cholinergic synapse；Melanogenesis；Hepatitis B；Viral carcinogenesis；Tight junction；Neurotrophin signaling pathway；GnRH signaling pathway；Gap junction；Glioma；T cell receptor signaling pathway； Alcoholism；Prostate cancer；Serotonergic synapse；Bladder cancer；Non-small cell lung cancer；Chronic myeloid leukemia；HTLV-I infection；B cell receptor signaling pathway；Pathways in cancer；Aldosterone-regulated sodium reabsorption；Colorectal cancer；Melanoma；Acute myeloid leukemia；Proteoglycans in cancer；Pancreatic cancer；Renal cell carcinoma；Thyroid cancer；Fc epsilon RI signaling pathway

Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumor oncogene KRAS and implicate that lncRNA-NUTF2P3-001 and miR-3923 can be applied as novel predictors and therapeutic targets for pancreatic cancer.

Hypoxia-induced lncRNA-NUTF2P3-001 contributes to tumorigenesis of pancreatic cancer by derepressing the miR-3923/KRAS pathway