Prostate cancer (PCa) has become the second leading cause of cancer-related mortality in males worldwide. Although the long noncoding RNA DLX6-AS1 has been recognized to be an oncogene in multiple cancers, the biological function and regulatory mechanism of DLX6-AS1 in prostate cancer are still obscure. In the present study, we observed that DLX6-AS1 was significantly upregulated in PCa tissues and cells. Knockdown of DLX6-AS1 inhibited PCa progression by suppressing cell proliferation and accelerating cell apoptosis. Molecular mechanism exploration indicated that DLX6-AS1 acted as a sponge for miR-497-5p and synuclein gamma (SNCG) was a downstream target gene of miR-497-5p. In addition, there was a negative correlation between DLX6-AS1 and miR-497-5p in PCa tissues. Rescue assays showed that SNCG overexpression could partially recover DLX6-AS1 knockdown-mediated inhibition of progression in PCa. Furthermore, xenograft tumor model was established to determine the role of DLX6-AS1 in PCa tumor growth and the results suggested that DLX6-AS1 could facilitate tumor growth by regulating SNCG in vivo. In conclusion, our study investigated the biological function and underlying mechanism of DLX6-AS1 in PCa and validated that DLX6-AS1 functioned as an oncogene through miR-497-5p/SNCG axis.

中文翻译：

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DLX6-AS1通过调节前列腺癌中的miR-497-5p/SNCG通路加速细胞增殖

前列腺癌 (PCa) 已成为全球男性癌症相关死亡的第二大原因。尽管长链非编码RNA DLX6-AS1已被认为是多种癌症的致癌基因，但DLX6-AS1在前列腺癌中的生物学功能和调控机制仍不清楚。在本研究中，我们观察到 DLX6-AS1 在 PCa 组织和细胞中显着上调。敲低 DLX6-AS1 通过抑制细胞增殖和加速细胞凋亡来抑制 PCa 进展。分子机制探索表明DLX6-AS1作为miR-497-5p的海绵，突触核蛋白γ（SNCG）是miR-497-5p的下游靶基因。此外，PCa组织中DLX6-AS1与miR-497-5p呈负相关。救援分析表明，SNCG 过表达可以部分恢复 DLX6-AS1 敲低介导的 PCa 进展抑制。此外，建立异种移植肿瘤模型以确定 DLX6-AS1 在 PCa 肿瘤生长中的作用，结果表明 DLX6-AS1 可以通过在体内调节 SNCG 促进肿瘤生长。总之，我们的研究调查了 DLX6-AS1 在 PCa 中的生物学功能和潜在机制，并通过 miR-497-5p/SNCG 轴验证了 DLX6-AS1 作为致癌基因发挥作用。