Long noncoding RNA, RNA component of mitochondrial RNA processing endoribonuclease (RMRP) plays an important role in cancer development and is closely correlated with prognosis in cancer patients. However, whether RMRP affects prognosis in patients with hepatocellular carcinoma (HCC) remains unclear. The aim of the present study was to investigate the expression level of RMRP in HCC and its correlation with prognosis in patients with HCC and explain the effects and associated mechanisms by conducting an in vitro study. The high expression level of RMRP was correlated with poor prognosis in patients with HCC. Using in vitro analysis, RMRP knockdown suppressed HCC cell proliferation, invasion, and migration (P < .05). miRNA‐206 overexpression had similar effects in HCC cell lines (Bel‐7402 and Huh‐7). Using Western blot analysis and cellular immunofluorescence detection, RMRP downregulation significantly suppressed TACR1/Erk1/2 pathway, while miRNA‐206 was significantly upregulated (P < .05). RMRP downregulation inhibits HCC‐related biological activities by the regulation of miRNA‐206/TACR1.

Articular cartilage (AC), a bone-to-bone protective device made of up to 80% water and populated by only one cell type (i.e. chondrocyte), has limited capacity for regeneration and self-repair after being damaged because of its low cell density, alymphatic and avascular nature. Resulting repair of cartilage defects, such as osteoarthritis (OA), is highly challenging in clinical treatment. Fortunately, the development of tissue engineering provides a promising method for growing cells in cartilage regeneration and repair by using hydrogels or the porous scaffolds. In this paper, we review the therapeutic strategies for AC defects, including current treatment methods, engineering/regenerative strategies, recent advances in biomaterials, and present emphasize on the perspectives of gene regulation and therapy of noncoding RNAs (ncRNAs), such as circular RNA (circRNA) and microRNA (miRNA).

Background Hepatocellular carcinoma (HCC) is a type of primary liver cancer with high mortality. Circular RNAs (circRNAs) have been confirmed to be involved in the development of HCC, but the functions of circ_0011232 in HCC remain ill‐defined. Methods Quantitative real‐time polymerase chain reaction, western blot assay, or immunohistochemistry assay was performed to determine the levels of circ_0011232, miR‐503‐5p, and AKT3. RNase R assay and actinomycin D assay were conducted to analyze the feature of circ_0011232. Cell Counting Kit‐8 assay, 5‐ethynyl‐2′‐deoxyuridine assay, colony formation assay, flow cytometry analysis, wound‐healing assay, and transwell assay were conducted to evaluate HCC cell proliferation, colony formation, apoptosis, migration, and invasion. Dual‐luciferase reporter assay was carried out to confirm the relationships among circ_0011232, miR‐503‐5p, and AKT3. The murine xenograft assay was conducted to verify the function of circ_0011232 in tumor growth in vivo. Results Circ_0011232 and AKT3 were upregulated, while miR‐503‐5p was decreased in HCC tissues and cells. Circ_0011232 knockdown repressed HCC cell proliferation, colony formation, migration, and invasion, and promoted apoptosis in vitro and blocked tumor growth in vivo. MiR‐503‐5p was a target of circ_0011232. MiR‐503‐5p inhibition reversed the effects of circ_0011232 knockdown on HCC cell development. Moreover, AKT3 was confirmed to be a target of miR‐503‐5p, and AKT3 overexpression abolished the inhibitory effects on HCC cell progression caused by miR‐503‐5p. Conclusion Circ_0011232 facilitated HCC progression via miR‐503‐5p/AKT3 axis, which might provide a novel treatment strategy for HCC.