Objective <p>Long non-coding RNA CASC15 plays a role in the development of various human diseases. However, the diagnostic role and molecular mechanisms of CASC15 in postmenopausal osteoporosis (PMOP) remain unclear.</p> Methods <p>This study enrolled 137 healthy postmenopausal women and 141 PMOP patients. CASC15 and miR-152-3p levels in serum and HBMSCs were measured via RT-qPCR. Western blotting and RT-qPCR were employed to analyze the protein and mRNA expression levels of osteogenic markers (RUNX2, ALP, OCN, Col I). CASC15’s diagnostic value was assessed by the ROC curve. Proliferation (CCK-8) and apoptosis (flow cytometry) were examined. CASC15-miR-152-3p targeting was confirmed via DLR and RIP assays.</p> Results <p>CASC15 expression was increased, while miR-152-3p expression was decreased in PMOP. CASC15 expression levels were higher in PMOP patients with fractures, and this molecule effectively distinguished between healthy individuals and PMOP patients, as well as between those with and without fractures. Functional experiments showed that inhibiting CASC15 enhanced HBMSCs’ proliferation and osteogenic differentiation capacity while reducing apoptosis. However, inhibiting miR-152-3p reversed these effects.</p> Conclusion <p>The level of CASC15 is closely linked to the occurrence and development of fractures in PMOP patients. Its molecular mechanism may involve targeting miR-152-3p to restrict its levels, thereby reducing osteogenic differentiation in HBMSCs.</p>

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LncRNA CASC15 serves as a diagnostic biomarker for postmenopausal osteoporotic fractures and its knockdown enhances HBMSC osteogenic differentiation via miR-152-3p

  • Xuri Wu,
  • Weiyang Zhang,
  • Jingjing Liu,
  • Ke Ma,
  • Shengqian Wang,
  • Zhibiao Wang,
  • Xinxin Ding

摘要

Objective

Long non-coding RNA CASC15 plays a role in the development of various human diseases. However, the diagnostic role and molecular mechanisms of CASC15 in postmenopausal osteoporosis (PMOP) remain unclear.

Methods

This study enrolled 137 healthy postmenopausal women and 141 PMOP patients. CASC15 and miR-152-3p levels in serum and HBMSCs were measured via RT-qPCR. Western blotting and RT-qPCR were employed to analyze the protein and mRNA expression levels of osteogenic markers (RUNX2, ALP, OCN, Col I). CASC15’s diagnostic value was assessed by the ROC curve. Proliferation (CCK-8) and apoptosis (flow cytometry) were examined. CASC15-miR-152-3p targeting was confirmed via DLR and RIP assays.

Results

CASC15 expression was increased, while miR-152-3p expression was decreased in PMOP. CASC15 expression levels were higher in PMOP patients with fractures, and this molecule effectively distinguished between healthy individuals and PMOP patients, as well as between those with and without fractures. Functional experiments showed that inhibiting CASC15 enhanced HBMSCs’ proliferation and osteogenic differentiation capacity while reducing apoptosis. However, inhibiting miR-152-3p reversed these effects.

Conclusion

The level of CASC15 is closely linked to the occurrence and development of fractures in PMOP patients. Its molecular mechanism may involve targeting miR-152-3p to restrict its levels, thereby reducing osteogenic differentiation in HBMSCs.