The function of linc-ROR exerted in LAD cells depended on the sponging of miR-145, therefore, releasing the miR-145 target FSCN1, and thus contributing to the acquisition of chemoresistance and EMT phenotypes of docetaxel-resistant LAD cells.

Long noncoding RNA ROR regulates chemoresistance in docetaxel-resistant lung adenocarcinoma cells via epithelial mesenchymal transition 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

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

Hippo signaling pathway

The experimental results indicate that lncRNA-ROR effectively maintains Sox2 gene expression through competitive binding to miR-145, achieving pluripotency maintenance in HuAECs and regulation of their directed β islet-like cell differentiation efficiency.

miR-145 modulates lncRNA-ROR and Sox2 expression to maintain human amniotic epithelial stem cell pluripotency and β islet-like cell differentiation efficiency

Transcriptional misregulation in cancer

Compared with the MCF7 cells, the MCF7-ROR cells had remarkably higher proliferation rates, down-regulated E-cadherin and miR-205 expressions, as well as increased vimentin, invasive ability, and mRNA expression of ZEB1 and ZEB2. Compared with the MCF7/TR5 and MDA-MB-231 cells, up-regulated E-cadherin and miR-205 expression, down-regulated expression of vimentin, ZEB1, and ZEB2 mRNA, and decreased invasive ability were observed in the MCF7/TR5 ROR-siRNA and MDA-MB-231 ROR-siRNA cells.

Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205

Specifically, linc-ROR prevented the degradation of mir-205 target genes, including the EMT inducer ZEB2.

LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis

Compared with the MCF7 cells, the MCF7-ROR cells had remarkably higher proliferation rates, down-regulated E-cadherin and miR-205 expressions, as well as increased vimentin, invasive ability, and mRNA expression of ZEB1 and ZEB2. Compared with the MCF7/TR5 and MDA-MB-231 cells, up-regulated E-cadherin and miR-205 expression, down-regulated expression of vimentin, ZEB1, and ZEB2 mRNA, and decreased invasive ability were observed in the MCF7/TR5 ROR-siRNA and MDA-MB-231 ROR-siRNA cells.

Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205