This study aimed to characterize the expression status and potentially mechanistic involvement of SNHG7 in pituitary adenoma. Relative expression of SNHG7 and miR-449a was analyzed by real-time PCR. Cell viability was measured with Cell Counting Kit-8 (CCK-8). Cell apoptosis was determined by PI/Annexin V double staining followed by flow cytometry analysis. Cell invasion and migration were analyzed by wound healing and transwell assays, respectively. The regulatory action of miR-449a on SNHG7 was interrogated by luciferase reporter assay. We also investigated the pro-tumor activity of SNHG7 with the MMQ xenograft tumor mouse model. We identified the aberrant up-regulation of SNHG7 in pituitary adenoma both in vivo and in vitro, which associated with poor survival outcome. siRNA-mediated SNHG7-knockdown decreased cell viability, increased apoptosis and compromised migration and invasion. We further predicted and validated that SNHG7 negatively regulated miR-449a via sponging. Concurrent inhibition of miR-449a restored cell viability, apoptosis, migration and invasion influenced by SNHG7-deficiency. Most importantly, we demonstrated that SNHG7-silencing delayed xenograft tumor progression, which was accompanied with increased miR-449a and decreased Ki67 intensity. Our study highlighted the essential oncogenic properties of the SNHG7/miR-449a axis in pituitary adenoma.

本研究旨在表征 SNHG7 在垂体腺瘤中的表达状态和潜在的机制参与。通过实时PCR分析SNHG7和miR-449a的相对表达。使用细胞计数试剂盒-8 (CCK-8) 测量细胞活力。通过PI/Annexin V双染色随后流式细胞术分析确定细胞凋亡。分别通过伤口愈合和 transwell 测定分析细胞侵袭和迁移。miR-449a 对 SNHG7 的调节作用通过荧光素酶报告基因测定进行了询问。我们还使用 MMQ 异种移植肿瘤小鼠模型研究了 SNHG7 的促肿瘤活性。我们在体内和体外鉴定了垂体腺瘤中 SNHG7 的异常上调，这与较差的生存结果相关。siRNA 介导的 SNHG7 敲低降低了细胞活力，增加细胞凋亡并损害迁移和侵袭。我们进一步预测并验证了 SNHG7 通过海绵作用负调控 miR-449a。同时抑制 miR-449a 可恢复受 SNHG7 缺陷影响的细胞活力、凋亡、迁移和侵袭。最重要的是，我们证明了 SNHG7 沉默延迟了异种移植肿瘤的进展，伴随着 miR-449a 的增加和 Ki67 强度的降低。我们的研究强调了垂体腺瘤中 SNHG7/miR-449a 轴的基本致癌特性。我们证明了 SNHG7 沉默延迟了异种移植肿瘤的进展，伴随着 miR-449a 的增加和 Ki67 强度的降低。我们的研究强调了垂体腺瘤中 SNHG7/miR-449a 轴的基本致癌特性。我们证明了 SNHG7 沉默延迟了异种移植肿瘤的进展，伴随着 miR-449a 的增加和 Ki67 强度的降低。我们的研究强调了垂体腺瘤中 SNHG7/miR-449a 轴的基本致癌特性。