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

Activity of the p53/miR-145 pathway may help explain the role of lincRNA-ROR for stress-induced regulation in CRC therapy.

The long noncoding RNA-ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the p53/miR-145 pathway

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

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

Further, we identify that p53 transcriptionally activates NRF expression. P53 regulates cardiomyocytes necrosis and myocardial I/R injury through NRF and miR-873.

The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873