Department of Spine Surgery, Zhujiang Hosptial, Southern Medical University, Guangzhou, China.
Department of Rehabilitation Medicine, The First Affiliated Hospital of Gannan Medical College, Ganzhou, China.
Technol Cancer Res Treat. 2024 Jan-Dec;23:15330338241261616. doi: 10.1177/15330338241261616.
To investigate the effects and the related signaling pathway of miR-362-3p on OS. The bioinformatics analysis approaches were employed to investigate the target pathway of miR-362-3p. After the 143B and U2OS cells and nu/nu male mice were randomly divided into blank control (BC) group, normal control (NC) group, and overexpression group (OG), the CCK-8, EdU staining, wound healing assay, Transwell assay, and TUNEL staining were adopted to respectively determine the effects of overexpressed miR-362-3p on the cell viability, proliferation, migration, invasion, and apoptosis of 143B and U2OS cells , tumor area assay and hematoxylin and eosin staining were employed to respectively determine the effects of overexpressed miR-362-3p on the growth and pathological injury of OS tissue . The qRT-PCR, Western blot, and immunohistochemical staining were applied to respectively investigate the effects of overexpressed miR-362-3p on the IL6ST/JAK2/STAT3 pathway in OS and . The bioinformatics analysis approaches combined qRT-PCR indicated that the IL6ST/JAK2/STAT3 is one of the target pathways of miR-362-3p. Compared with NC, the cell viability, proliferation, migration, and invasion of 143B and U2OS cells were dramatically (< 0.01) inhibited but the apoptosis was prominently (<0 .0001) promoted in OG. Compared with NC, the growth of OS tissue was significantly (< 0.05) suppressed and the pathological injury of OS tissue was substantially aggravated in OG. The gene expression levels of IL6ST, JAK2, and STAT3 and the protein expression levels of IL6ST, JAK2, p-JAK2, STAT3, and p-STAT3 in 143B and U2OS cells were memorably (< 0.0001) lower in OG than those in NC. In addition, the positively stained areas of proteins of IL6ST, JAK2, p-JAK2, STAT3, and p-STAT3 of OS tissue in OG were markedly (< 0.01) reduced compared with those in NC. The overexpression of miR362-3p alleviates OS by inhibiting the IL6ST/JAK2/STAT3 pathway and .
探讨 miR-362-3p 对骨肉瘤（OS）的影响及其相关信号通路。采用生物信息学分析方法探讨 miR-362-3p 的靶通路。将 143B 和 U2OS 细胞及裸鼠分为空白对照组（BC 组）、正常对照组（NC 组）和过表达组（OG 组），采用 CCK-8、EdU 染色、划痕愈合实验、Transwell 实验和 TUNEL 染色分别检测过表达 miR-362-3p 对 143B 和 U2OS 细胞活力、增殖、迁移、侵袭和凋亡的影响，采用肿瘤面积检测和苏木精-伊红（H&E）染色分别检测过表达 miR-362-3p 对 OS 组织生长和病理损伤的影响，采用 qRT-PCR、Western blot 和免疫组化染色分别检测过表达 miR-362-3p 对 OS 中 IL6ST/JAK2/STAT3 通路的影响。生物信息学分析联合 qRT-PCR 表明，IL6ST/JAK2/STAT3 是 miR-362-3p 的靶通路之一。与 NC 组相比，OG 组 143B 和 U2OS 细胞活力、增殖、迁移和侵袭显著（<0.01）下降，凋亡明显（<0.0001）增加。与 NC 组相比，OG 组 OS 组织生长明显（<0.05）受抑制，OS 组织病理损伤显著加重。与 NC 组相比，OG 组 143B 和 U2OS 细胞中 IL6ST、JAK2、STAT3 基因表达水平及 IL6ST、JAK2、p-JAK2、STAT3、p-STAT3 蛋白表达水平均显著（<0.0001）降低。此外，OG 组 OS 组织中 IL6ST、JAK2、p-JAK2、STAT3 和 p-STAT3 蛋白阳性染色面积均明显（<0.01）低于 NC 组。过表达 miR362-3p 通过抑制 IL6ST/JAK2/STAT3 通路减轻 OS。
