HIF-1 signaling pathway； MAPK signaling pathway； Endometrial cancer；Glioma；ErbB signaling pathway；Calcium signaling pathway；Cytokine-cytokine receptor interaction；Proteoglycans in cancer；Prostate cancer；Endocytosis；GnRH signaling pathway；PI3K-Akt signaling pathway；Dorso-ventral axis formation；Non-small cell lung cancer；Pancreatic cancer；Melanoma；Bladder cancer；Focal adhesion；Hepatitis C；Adherens junction；Gap junction；Epithelial cell signaling in Helicobacter pylori infection；Regulation of actin cytoskeleton；Pathways in cancer；Estrogen signaling pathway

Moreover, as exhibited by luciferase reporter gene assays, miR-133a bound to XIST and the 3'UTR of EGFR by direct targeting.

LncRNA XIST Promotes Pancreatic Cancer Proliferation through miR-133a/EGFR

Further experiments revealed that overexpressed TUG1 promoted cell proliferation, migration and contributed to EMT formation, whereas silenced TUG1 led to opposing results. Additionally, luciferase reporter assays, an RIP assay and an RNA-pulldown assay demonstrated that TUG1 could competitively sponge miR-382 and thereby regulate EZH2.

The Lncrna-TUG1/EZH2 Axis Promotes Pancreatic Cancer Cell Proliferation, Migration and EMT Phenotype Formation Through Sponging Mir-382.

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

Jak-STAT signaling pathway；Natural killer cell mediated cytotoxicity；Leukocyte transendothelial migration；Neurotrophin signaling pathway；Adipocytokine signaling pathway；Epithelial cell signaling in Helicobacter pylori infection；Herpes simplex infection；Proteoglycans in cancer；Renal cell carcinoma；Chronic myeloid leukemia

LINC00673 is able to reinforce the interaction of PTPN11 with PRPF19, an E3 ubiquitin ligase, and promote PTPN11 degradation through ubiquitination, which causes diminished SRC-ERK oncogenic signaling and enhanced activation of the STAT1-dependent antitumor response. A G>A change at rs11655237 in exon 4 of LINC00673 creates a target site for miR-1231 binding, which diminishes the effect of LINC00673 in an allele-specific manner and thus confers susceptibility to tumorigenesis.

Pancreatic cancer risk variant in LINC00673 creates a miR-1231 binding site and interferes with PTPN11 degradation