Dopaminergic synapse；PI3K-Akt signaling pathway；HTLV-I infection；Huntington's disease；Hepatitis B；Osteoclast differentiation；Antigen processing and presentation；Circadian rhythm；Alcoholism；Circadian entrainment；Cholinergic synapse；Prostate cancer；Viral carcinogenesis；Cocaine addiction；Tuberculosis；Insulin secretion；Estrogen signaling pathway；Melanogenesis；Amphetamine addiction；Vasopressin-regulated water reabsorption

Moreover, UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1

Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells

Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA.

LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2

Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).

Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN3 pathway

ErbB signaling pathway；HIF-1 signaling pathway；Cell cycle；PI3K-Akt signaling pathway；Chronic myeloid leukemia；Hepatitis B； Measles； Epstein-Barr virus infection；Small cell lung cancer；Pathways in cancer；Transcriptional misregulation in cancer； Viral carcinogenesis；Prostate cancer

Among these 8 candidant miRNAs, we observed the correlation among UCA1, miR-196a and the host target mRNA, p27kip1, in bladder cancer cells and tissues.

Gene expression profiling of microRNAs associated with UCA1 in bladder cancer cells

MAPK signaling pathway；Cell cycle；Epstein-Barr virus infection；p53 signaling pathway；PI3K-Akt signaling pathway；Apoptosis；Thyroid cancer；Melanoma；Basal cell carcinoma；Measles；Chronic myeloid leukemia；Wnt signaling pathway；Neurotrophin signaling pathway；HTLV-I infection；Non-small cell lung cancer；Proteoglycans in cancer；Prostate cancer；Amyotrophic lateral sclerosis (ALS)；Transcriptional misregulation in cancer；Pathways in cancer；Pancreatic cancer；Huntington's disease；Hepatitis C；Colorectal cancer；Glioma；Bladder cancer；Endometrial cancer；Hepatitis B；Viral carcinogenesis；Small cell lung cancer；Herpes simplex infection

Ectopic expression of H19 significantly increased bladder cancer cell proliferation and miR-675 expression in vitro. Furthermore, overexpression of miR-675 promoted bladder cancer cell proliferation, while suppression of miR-675 induced G1 phase cell cycle arrest and promoted cell apoptosis. Western blotting analysis further identified that miR-675 inhibited p53 activation, decreased the ratio of Bax/Bcl-2 and cyclin D1 expression in bladder cancer cells； those effects may result in the abnormal proliferation of bladder cancer cells.

H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation

Transcriptional misregulation in cancer

Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).

Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway

Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).

Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN2 pathway