研究人员发现了一个与癌症相关骨骼损失相关的蛋白质路径,并发现了可以保护病人骨骼的药物。 Researchers found a protein pathway linked to cancer-related bone loss and identified drugs that may protect bones in patients.

美国内布拉斯加大学医学中心的研究人员发现, 解折蛋白反应 (UPR) 途径是治疗癌症患者骨衰弱的有希望的目标. Researchers at the University of Nebraska Medical Center have identified the unfolded protein response (UPR) pathway as a promising target for treating bone weakening in cancer patients. 控制内细胞网中的压力, UPR 经常在多发性骨髓瘤,乳腺和前列腺转移以及骨瘤等癌症中被破坏,导致骨重塑失衡,骨损失增加,骨折风险增加. The UPR, which manages stress in the endoplasmic reticulum, is often disrupted in cancers like multiple myeloma, breast and prostate metastases, and bone tumors, leading to imbalanced bone remodeling, increased bone loss, and higher fracture risk. 通过准关键的UPR蛋白质,如EIF2AK3,ERN1和ATF6,科学家们的目标是恢复骨强度,减少与骨相关的事件. By targeting key UPR proteins such as EIF2AK3, ERN1, and ATF6, scientists aim to restore bone strength and reduce skeletal-related events. 几种实验药物如苏尼替尼,乙酸,龙酸和在早期研究中显示出抑制有害的UPR信号,改善蛋白质折叠或杀死骨癌细胞的潜力. Several experimental drugs—like sunitinib, sodium phenylbutyrate, zoledronic acid, and oprozomib—show potential in early studies by inhibiting harmful UPR signals, improving protein folding, or killing cancer cells in bone. 然而,在制订保护健康组织同时有效治疗癌症引起的骨骼疾病的选择性治疗办法方面仍然存在挑战。 However, challenges remain in developing selective treatments that protect healthy tissue while effectively treating cancer-induced bone disease. 需要进行进一步的研究,以确认人类的安全性和有效性。 Further research is needed to confirm safety and effectiveness in humans.