The Subcellular Localization of IncRNA FAM230B in Osteosarcoma and Its Interaction with Early miR-203.

Previous studies have revealed the role of lncRNA FAM230B in promoting papillary thyroid cancer and gastric cancer. We predicted that FAM230B may interact with miR-203 and studied the crosstalk between FAM230B and miR-203 in osteosarcoma (OS). Paired OS and nontumor tissues donated by 60 patients with OS were subjected to RNA isolations and quantitative real-time PCR (RT-qPCR) to analyze the expression of both FAM230B and miR-203 (mature and premature levels). Subcellular location of FAM230B in OS cells was detected using subcellular fractionation assay. RNA pull-down assay was performed to investigate the direct interaction between FAM230B and miR-203. Overexpression assays followed by RT-qPCR were performed to analyze the role of FAM230B in miR-203 maturation. Cell proliferation was studied with 5-Bromo-2-deoxyUridine (BrdU) assay. FAM230B and premature miR-203 were upregulated in OS, whereas mature miR-203 was downregulated in OS cells. FAM230B was detected in the cytoplasm and directly interacted with premature miR-203. FAM230B overexpression in OS cells increased premature miR-203 level and decreased mature miR-203 level. FAM230B increased cell proliferation and suppressed the role of miR-203 in inhibiting cell proliferation. FAM230B in the cytoplasm may sponge premature miR-203, thereby inhibiting miR-203 maturation to increase OS cell proliferation.

MicroRNA-492 overexpression exerts suppressive effects on the progression of osteosarcoma by targeting PAK7.

MicroRNAs (miRNAs or miRs), which are a class of non-coding RNAs, have emerged as effective modulators of various aspects of biological processes. Accumulating evidence has established significant associations between the dysregulation of miRs and tumorigenesis in various types of cancer. However, the role of miR­492, particularly in osteosarcoma (OS) remains elusive. In present study, we demonstrated that miR­492 functions as putative tumor suppressor miR in OS. The level of miR­492 was frequently downregulated in both OS tissues and cell lines. Moreover, the ectopic overexpression of miR­492 effectively inhibited the proliferation, migration and invasion of OS cell lines. Furthermore, transfection with a miR­492 overexpression vector also strongly attenuated the growth of xenograft tumors in vivo. p21-activated kinase (PAK7) was identified as the putative target of miR­492 in OS, and we further found a significantly inverse correlation between PAK7 and miR­492 in OS specimens. Taken together, our study has unraveled a novel role for miR­492 in OS and may help in establishing the rationale for more effective treatment strategies for OS via miR regulation.