基因敲除
下调和上调
微量注射
脊髓
小发夹RNA
痛觉过敏
医学
背
癌症研究
伤害
细胞生物学
化学
药理学
神经科学
内科学
生物
解剖
受体
基因
生物化学
作者
Jiao Kuang,Miao Xu,Chengfei Xu,Yahui Wang,Chaobo Ni,Shirong Wei,Zhihao Liu,Min Kong,Qinghe Zhou,Ming Yao,Huadong Ni
标识
DOI:10.1016/j.bbrc.2023.09.069
摘要
Due to its complex pathological mechanisms, bone cancer pain (BCP) has become an increasingly challenging clinical issue, there is an urgent need to identify the underlying mechanisms of BCP. In our present study, we found that decreased expression of miR-199a-3p in spinal dorsal horn (SDH) neurons contributed to BCP hypersensitivity. Intrathecal administration of miR-199a-3p agomir alleviated the initiation of tumor inoculation induced pain hypersensitivity and suppressed the expression of DNMT3A. Subsequently, luciferase assays confirmed direct binding between miR-199a-3p and Dnmt3a mRNA. AAV-DNMT3A-shRNA microinjection relieved mechanical hyperalgesia and upregulated the expression of Nrf2 levels in BCP. In naïve rats, Overexpression of DNMT3A yielded the opposite effects. Finally, increase of DNMT3A by lentiviral vector abolished miR-199a-3p-mediated alleviation hypersensitivity effects on BCP progression. Taken these together, our findings highlighted a novel contribution of miR‐199a-3p to BCP and provided a fresh outlook on potential mechanism research for BCP.
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