Abstract Glioma is a malignant primary brain tumor that occurs in the central nervous system and has threatened the well-being of millions of patients. It is well acknowledged that long non-coding RNA (lncRNA) SNHG3 participates in the regulation of proliferation, inflation, differentiation, and metastasis in many cancers. However, the regulatory effect of SNHG3 on glioma progression is still controversial. The expression of SNHG3 and HDGF was upregulated, whereas miR-384 was downregulated in glioma tissues, compared with the normal tissues. Interestingly, high SNHG3 contributed to low survival rate while low SNHG3 showed the opposite result. Moreover, SNHG3 or HDGF knockdown significantly suppressed proliferation, migration, and invasion and induced apoptosis in glioma. Meanwhile, restoration of HDGF abrogated the inhibition of SNHG3 silencing on glioma cell progression. Besides, miR-384 inhibitor attenuated SNHG3 silencing induced inhibition on HDGF mRNA and protein expression in A172 and SHG44 cells. LncRNA SNHG3 promotes cell proliferation, migration, and invasion in glioma by enhancing HDGF expression via miR-384 sponging, representing the promising targets for the development of novel therapeutic strategies.

中文翻译：

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长链非编码 RNA SNHG3 通过调节 miR-384/HDGF 轴加速胶质瘤进展

摘要 胶质瘤是一种发生于中枢神经系统的恶性原发性脑肿瘤，已威胁到数百万患者的健康。众所周知，长链非编码 RNA (lncRNA) SNHG3 参与调节许多癌症的增殖、膨胀、分化和转移。然而，SNHG3对胶质瘤进展的调节作用仍存在争议。与正常组织相比，神经胶质瘤组织中 SNHG3 和 HDGF 的表达上调，而 miR-384 的表达下调。有趣的是，高 SNHG3 导致低存活率，而低 SNHG3 显示相反的结果。此外，SNHG3 或 HDGF 敲低显着抑制胶质瘤的增殖、迁移和侵袭并诱导细胞凋亡。同时，HDGF 的恢复消除了 SNHG3 沉默对神经胶质瘤细胞进展的抑制。此外，miR-384 抑制剂减弱了 SNHG3 沉默对 A172 和 SHG44 细胞中 HDGF mRNA 和蛋白质表达的抑制。LncRNA SNHG3 通过 miR-384 海绵增强 HDGF 表达促进神经胶质瘤中的细胞增殖、迁移和侵袭，代表了开发新治疗策略的有希望的靶点。