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Background: It is known that long non-coding RNA (lncRNA) PTCSC3 is involved in thyroid cancer and glioma, but its function in osteoporosis is unknown. The aim of our study was to investigate the role of lncRNA PTCSC3 in osteoporosis. Methods: A total of 80 patients with osteoporosis (4 clinical stages) and four corresponding groups of healthy controls were enrolled. Plasma PTCSC3 levels in the 80 osteoporosis patients and 80 healthy volunteers were measured using RT-qPCR. The diagnostic potential of plasma PTCSC3 for osteoporosis was evaluated by ROC curve analysis with healthy volunteers as the true negative cases and corresponding osteoporosis patients as the true positive cases. Results: PTCSC3 was upregulated in osteoporosis patients compared with healthy controls. PTCSC3 levels increased with osteoporosis stages increasing, but not with healthy controls aging. PTCSC3 overexpression separated each stage of osteoporosis from corresponding controls. PTCSC3 overexpression promoted while PTCSC3 silencing inhibited osteoblast apoptosis. However, PTCSC3 overexpression and silencing showed no significant effect on osteoclast apoptosis. LncRNA PTCSC3 was upregulated in osteoporosis and negatively regulated osteoblast apoptosis. Conclusion: LncRNA PTCSC3 may serve as a potential therapeutic target for osteoporosis. [ABSTRACT FROM AUTHOR]

The article titled "Retraction Note: LncRNA PTCSC3 is upregulated in osteoporosis and negatively regulates osteoblast apoptosis" has been retracted by the editors of BMC Medical Genomics. The retraction was made due to significant overlap with an unpublished manuscript by different authors that was previously submitted to a different journal. The authors did not respond to requests for clarification or correspondence regarding the retraction. Springer Nature, the publisher, remains neutral in terms of jurisdictional claims and institutional affiliations. The authors of the retracted article are Xingchao Liu, Mingliang Chen, Qinghe Liu, Gang Li, Pei Yang, and Guodong Zhang. [Extracted from the article]

Recently, the role of microRNAs (miRs) in human diseases has been verified. This study was determined to explore the protective effects of microRNA-26a (miR-26a) in steroid-induced osteonecrosis of the femoral head (SONFH) with the involvement of enhancer of zeste homologue 2 (EZH2). Femoral head (FH) samples from SONFH patients and patients with femoral neck fracture were collected, and rat SONFH models were established by Escherichia coli endotoxin combining with large dose steroid pulse assay. The hemorheology, blood lipid, inflammatory factors, and pathologic changes were measured by a series of experiments. Moreover, the detection of osteoblasts, osteoclasts, miR-26a expression, EZH2 expression, osteoprotegerin (OPG) and osteoprotegerin ligand (OPGL), and the apoptosis of osteocytes were conducted. The target relation between miR-26a and EZH2 was clarified by bioinformatics and dual-luciferase reporter gene assay. MiR-26a was poorly expressed, while EZH2 was highly expressed in SONFH, and the elevation of miR-26a could repress EZH2 expression. Elevated miR-26a and reduced EZH2 were able to decelerate the apoptosis of osteocytes, increase osteoblasts, and decrease osteoclasts, resulting in a repression of SONFH progression. Additionally, EZH2 was a target gene of miR-26a. Furthermore, the elevation of EZH2 could reverse the repression of SONFH progression that is induced by elevated miR-26a. We found that up-regulation of miR-26a and knockdown of EZH2 could suppress the development of SONFH, which would contribute to the therapy of SONFH. [ABSTRACT FROM AUTHOR]