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Background <p>Osteoporosis (OP) represents a major global health challenge, particularly among postmenopausal women. Currently, there remains a shortage of reliable diagnostic biomarkers and targeted therapies for OP.</p> Methods <p>A cohort of 254 postmenopausal women (127 OP patients and 127 healthy controls) was analyzed. Serum miR-629-3p levels were measured via qRT-PCR, and diagnostic potential was assessed using ROC analysis. In vitro, MC3T3-E1 osteoblasts were transfected with miR-629-3p mimic/inhibitor and <i>BACH1</i> overexpression vector (oe-<i>BACH1</i>). Proliferation and apoptosis were evaluated by functional assays (CCK-8, Annexin V-FITC/PI staining), while osteogenic markers (FN1, ITGB1 and RUNX2) were assessed by qPCR. The binding of miR-629-3p to the <i>BACH1</i> 3’UTR was confirmed by luciferase reporter assays.</p> Results <p>Our findings revealed significantly decreased miR-629-3p levels in OP patients (<i>P</i> &lt; 0.001), negatively correlating with <i>BACH1</i> (<i>r</i> = -0.696, <i>P</i> &lt; 0.001) and showing diagnostic potential (AUC = 0.929). Mechanistically, miR-629-3p mimic suppressed <i>BACH1</i> (<i>P</i> &lt; 0.001), enhancing proliferation, reducing apoptosis, and upregulating RUNX2 (all <i>P</i> &lt; 0.001), while <i>BACH1</i> overexpression reversed these effects. Luciferase assays confirmed miR-629-3p directly targets <i>BACH1</i> 3’UTR (<i>P</i> &lt; 0.001).</p> Conclusion <p>miR-629-3p attenuates OP progression by inhibiting <i>BACH1</i>, thereby promoting osteoblast survival, proliferation, and differentiation. Its diagnostic potential and therapeutic role in restoring osteogenic function highlight miR-629-3p/<i>BACH1</i> as a promising axis for OP management. However, the findings of this study require further validation in animal models to fully establish causality.</p>

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miR-629-3p affects postmenopausal osteoporosis through targeted regulation of BACH1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月14日

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  • Dong Yun,
  • Jinxiang Zhang,
  • Siyuan Ha,
  • Jing Xiao,
  • Caifeng Yan

摘要

Background

Osteoporosis (OP) represents a major global health challenge, particularly among postmenopausal women. Currently, there remains a shortage of reliable diagnostic biomarkers and targeted therapies for OP.

Methods

A cohort of 254 postmenopausal women (127 OP patients and 127 healthy controls) was analyzed. Serum miR-629-3p levels were measured via qRT-PCR, and diagnostic potential was assessed using ROC analysis. In vitro, MC3T3-E1 osteoblasts were transfected with miR-629-3p mimic/inhibitor and BACH1 overexpression vector (oe-BACH1). Proliferation and apoptosis were evaluated by functional assays (CCK-8, Annexin V-FITC/PI staining), while osteogenic markers (FN1, ITGB1 and RUNX2) were assessed by qPCR. The binding of miR-629-3p to the BACH1 3’UTR was confirmed by luciferase reporter assays.

Results

Our findings revealed significantly decreased miR-629-3p levels in OP patients (P < 0.001), negatively correlating with BACH1 (r = -0.696, P < 0.001) and showing diagnostic potential (AUC = 0.929). Mechanistically, miR-629-3p mimic suppressed BACH1 (P < 0.001), enhancing proliferation, reducing apoptosis, and upregulating RUNX2 (all P < 0.001), while BACH1 overexpression reversed these effects. Luciferase assays confirmed miR-629-3p directly targets BACH1 3’UTR (P < 0.001).

Conclusion

miR-629-3p attenuates OP progression by inhibiting BACH1, thereby promoting osteoblast survival, proliferation, and differentiation. Its diagnostic potential and therapeutic role in restoring osteogenic function highlight miR-629-3p/BACH1 as a promising axis for OP management. However, the findings of this study require further validation in animal models to fully establish causality.