Department of Emergency Surgery, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou, Fujian 350001, PR China.
Department of Medical Oncology, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou, Fujian 350001, PR China.
Future Oncol. 2020 Apr;16(11):665-674. doi: 10.2217/fon-2019-0432. Epub 2020 Apr 6.
This experimental design was based on DHRS12 to explore its biological effects on osteosarcoma (OS). The expression level of endogenous DHRS12 was analyzed by immunohistochemical analysis. DHRS12 was overexpressed in MG-63 and HOS cells by plasmid transfection. Cell proliferation, invasion, migration, apoptosis and western blot were used in the experiment. The expression of DHRS12 was significantly reduced in OS. Overexpression of DHRS12 inhibited the proliferation, migration and invasion of MG-63 and HOS cells and induced apoptosis of OS cells. Overexpression of DHRS12 upregulated Bax, Caspase 9 and Caspase 3. Overexpression of DHRS12 resulted in inactivation of the Wnt3a/β-catenin signaling pathway. Overexpression of DHRS12 inhibited the progression of OS via the Wnt3a/β-catenin pathway.
本实验设计基于 DHRS12 来探讨其对骨肉瘤（OS）的生物学作用。通过免疫组织化学分析来分析内源性 DHRS12 的表达水平。通过质粒转染使 MG-63 和 HOS 细胞中 DHRS12 过表达。实验中采用细胞增殖、侵袭、迁移、凋亡和 Western blot。OS 中 DHRS12 的表达明显降低。DHRS12 的过表达抑制了 MG-63 和 HOS 细胞的增殖、迁移和侵袭，并诱导 OS 细胞凋亡。DHRS12 的过表达上调了 Bax、Caspase 9 和 Caspase 3。DHRS12 的过表达导致 Wnt3a/β-catenin 信号通路失活。DHRS12 的过表达通过 Wnt3a/β-catenin 通路抑制 OS 的进展。
