LncRNA ROR1-AS1 accelerates osteosarcoma invasion and proliferation through modulating miR-504
Related Experiment Video
Updated: Nov 22, 2025

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Xiangkun Wu1, Lihua Yan2, Yongxi Liu1
1Department of Orthopaedic Surgery, Nanyang Second People's Hospital, Nanyang 473000, Henan, China.
Abstract:
Long non-coding RNAs (LncRNAs) play vital roles in the progression and development of tumors. However, the functional role of ROR1-AS1 in osteosarcoma has not been investigated. We found that ROR1-AS1 was upregulated in osteosarcoma tissues compared to non-tumor samples. Elevated expression of ROR1-AS1 promoted cyclin D1, PCNA and ki-67 expression and increased cell cycle and growth in MG-63 cell. Moreover, overexpression of ROR1-AS1 induced cell migration in MG-63 cell, promoting N-cadherin and vimentin expression and inhibiting E-cadherin expression. Dual-luciferase assay proved that ROR1-AS1 served as one sponge for miR-504 and ROR1-AS1 overexpression suppressed miR-504 expression in MG-63 cell. ROR1-AS1 expression was lower in osteosarcoma tissues compared to non-tumor samples. Pearson's correlation assay showed a negative correlation between miR-504 and ROR1-AS1 expression. MiR-504 overexpression partly abrogated ROR1-AS1-induced effects on osteosarcoma cell migration and proliferation. These data implied that ROR1-AS1 played as an oncogene and might be a new treatment target for osteosarcoma.
Related Concept Videos
lncRNA - Long Non-coding RNAs
MicroRNAs
MicroRNAs
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
