Department of Obstetrics and Gynecology, Hangzhou Women's Hospital (Hangzhou Maternity and Child Health Care Hospital), Hangzhou, China.
Department of Gastrointestinal Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
J Cell Physiol. 2019 May;234(5):6624-6632. doi: 10.1002/jcp.27403. Epub 2018 Sep 24.
Increasing evidence showed that long noncoding RNAs (lncRNAs) played an important role in the occurrence and development of tumors. To date, lncRNA small nucleolar RNA host gene 12 (SNHG12) has revealed an oncogenic role in various tumors. However, the role of SNHG12 in cervical cancer is still unclear. Therefore, we focused on the biological function and molecular mechanism of SNHG12 in the tumorigenesis of cervical cancer. In this study, the expression of miR-125b was observably downregulated in cervical cancer cells. Meanwhile, the expression of SNHG12 was obviously upregulated in cervical cancer cell lines (HeLa, SiHa, Caski, C4-1, and C33A) compared with the immortalized cervical epithelial cells. The further assay showed that miR-125b was a target of SNHG12 in cervical cancer. Moreover, a negative relationship between miR-125b and SNHG12 was found in cervical cancer. In addition, SNHG12 inhibition restrained the proliferation, migration, and invasion of cervical cancer cells. Meanwhile, miR-125b mimics repressed the expression of signal transducer and activator of transcription 3 (STAT3). The further assay showed that STAT3 was a target of miR-125b in cervical cancer. In addition, sh-STAT3 repressed the migration and invasion of cervical cancer cells. Furthermore, it showed that miR-125b inhibitors reversed STAT3 expression restrained by the reduction of SNHG12 expression. In general, SNHG12 modulated STAT3 by sponging miR-125b in cervical cancer and played an important role in the development of cervical cancer.
越来越多的证据表明，长链非编码 RNA（lncRNA）在肿瘤的发生和发展中发挥着重要作用。迄今为止，lncRNA 核仁小分子 RNA 宿主基因 12（SNHG12）已在各种肿瘤中显示出致癌作用。然而，SNHG12 在宫颈癌中的作用尚不清楚。因此，我们专注于 SNHG12 在宫颈癌发生中的生物学功能和分子机制。在这项研究中，miR-125b 在宫颈癌细胞中的表达明显下调。同时，与永生化宫颈上皮细胞相比，SNHG12 在宫颈癌细胞系（HeLa、SiHa、Caski、C4-1 和 C33A）中表达明显上调。进一步的研究表明，miR-125b 是宫颈癌中 SNHG12 的靶基因。此外，在宫颈癌中发现 miR-125b 与 SNHG12 呈负相关。此外，SNHG12 抑制可抑制宫颈癌细胞的增殖、迁移和侵袭。同时，miR-125b 模拟物可抑制信号转导和转录激活因子 3（STAT3）的表达。进一步的研究表明，STAT3 是宫颈癌中 miR-125b 的靶基因。此外，sh-STAT3 抑制了宫颈癌细胞的迁移和侵袭。此外，研究表明，miR-125b 抑制剂逆转了 SNHG12 表达减少引起的 STAT3 表达抑制。总的来说，SNHG12 通过海绵吸附 miR-125b 调节 STAT3 在宫颈癌中的表达，在宫颈癌的发展中发挥着重要作用。
