Abstract：
BACKGROUND: Osteolytic bone metastasis is a common complication of Non-Small Cell Lung Cancer (NSCLC), resulting in bone pain, hypercalcemia, and fractures that severely reduce the quality of life and survival time of patients. Semaphorins 3A (Sema3A) is one of the isoforms of the Semaphorins family, which is important in a variety of physiological and pathological processes, such as angiogenesis, immune regulation, and tumorigenesis. However, the role of Sema3A in the development of osteolytic bone metastasis in NSCLC is unknown.
METHODS: In this study, we established in vitro models simulating NSCLC cells in regulating the differentiation and maturation of osteoblast and osteoclast precursors and observed the differentiation of osteoblasts and osteoclasts.
RESULTS: The results demonstrated that the expression of Sema3A inhibited the proliferation, migration, and invasion of NSCLC cells, as well as promoted the differentiation of osteoblasts and inhibited the differentiation of osteoclasts, suggesting that Sema3A can inhibit the occurrence and development of osteolytic bone metastasis of NSCLC.
CONCLUSIONS: This study provides a new idea for the clinical treatment of osteolytic bone metastasis in NSCLC.
METHODS: In this study, we established in vitro models simulating NSCLC cells in regulating the differentiation and maturation of osteoblast and osteoclast precursors and observed the differentiation of osteoblasts and osteoclasts.
RESULTS: The results demonstrated that the expression of Sema3A inhibited the proliferation, migration, and invasion of NSCLC cells, as well as promoted the differentiation of osteoblasts and inhibited the differentiation of osteoclasts, suggesting that Sema3A can inhibit the occurrence and development of osteolytic bone metastasis of NSCLC.
CONCLUSIONS: This study provides a new idea for the clinical treatment of osteolytic bone metastasis in NSCLC.
摘要：
背景：溶骨性骨转移是非小细胞肺癌（NSCLC）的常见并发症，导致骨痛，高钙血症,和严重降低患者生活质量和生存时间的骨折。信号素3A（Sema3A）是信号素家族的同种型之一，这在各种生理和病理过程中都很重要，比如血管生成，免疫调节，和肿瘤发生。然而,Sema3A在非小细胞肺癌溶骨性骨转移中的作用尚不清楚.
方法：在本研究中，我们建立了体外模拟NSCLC细胞调节成骨细胞和破骨细胞前体分化和成熟的模型，并观察了成骨细胞和破骨细胞的分化。
结果：结果表明Sema3A的表达抑制了细胞增殖，迁移,和NSCLC细胞的侵袭，以及促进成骨细胞的分化和抑制破骨细胞的分化,提示Sema3A可抑制NSCLC溶骨性骨转移的发生和发展。
结论：本研究为非小细胞肺癌溶骨性骨转移的临床治疗提供了新的思路。
方法：在本研究中，我们建立了体外模拟NSCLC细胞调节成骨细胞和破骨细胞前体分化和成熟的模型，并观察了成骨细胞和破骨细胞的分化。
结果：结果表明Sema3A的表达抑制了细胞增殖，迁移,和NSCLC细胞的侵袭，以及促进成骨细胞的分化和抑制破骨细胞的分化,提示Sema3A可抑制NSCLC溶骨性骨转移的发生和发展。
结论：本研究为非小细胞肺癌溶骨性骨转移的临床治疗提供了新的思路。
