This study aimed to reveal the potential roles of long non-coding RNA HCP5 (lncRNA HCP5) and its potential molecular mechanism in polycystic ovarian syndrome (PCOS). The human granulosa-like tumor cell line KGN was used for assessing the effects of HCP5 in the proliferation and apoptosis of granulosa cells (GCs). The results showed that downregulation of HCP5 suppressed cell proliferation through arresting cell cycle progression at G1 phase, and induced the apoptosis via activating mitochondrial pathway, while overexpression of HCP5 played the opposite effects in KGN cells. We predicted and confirmed miR-27a-3p was a directly target to HCP5 and it could directly bind with insulin-like growth factor-1 (IGF-1). Next, we performed gain- and loss-of-functions approaches by transfecting miR-27a-3p inhibitor into HCP5 knocking down cells and transfecting miR-27a-3p mimics into HCP5 overexpressing cells. The results demonstrated that downregulation and upregulation of miR-27a-3p could block the effects on the proliferation and apoptosis mediated by silencing and overexpressing HCP5 in KGN cells. Additionally, miR-27a-3p inhibitor remarkably reversed the IGF-1 decrease regulated by knocking down HCP5 and miR-27a-3p mimics inhibited the IGF-1 increase modulated by overexpressing HCP5 in KGN cells. Furthermore, we observed that the promoted cell vitality and reduced apoptosis mediated by enforced expression of HCP5 could be alleviated when the KGN cells transfected with IGF-1 siRNA. Our findings indicate that HCP5 might be a potential regulatory factor for development of PCOS through regulating the miR-27a-3p/IGF-1 axis.

中文翻译：

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LncRNA HCP5通过miR-27a-3p / IGF-1轴在人颗粒样肿瘤细胞KGN中促进细胞增殖并抑制细胞凋亡。

这项研究旨在揭示长非编码RNA HCP5（lncRNA HCP5）的潜在作用及其在多囊卵巢综合征（PCOS）中的潜在分子机制。使用人类颗粒样肿瘤细胞系KGN评估HCP5对颗粒细胞（GCs）增殖和凋亡的影响。结果表明，HCP5的下调通过在G1期阻止细胞周期进程来抑制细胞增殖，并通过激活线粒体途径诱导细胞凋亡，而HCP5的过表达在KGN细胞中起相反的作用。我们预测并证实miR-27a-3p是HCP5的直接靶标，并且可以直接与胰岛素样生长因子1（IGF-1）结合。下一个，我们通过将miR-27a-3p抑制剂转染到HCP5敲低细胞中并将miR-27a-3p模拟物转染到HCP5过表达的细胞中来执行功能获得和丧失的方法。结果表明，miR-27a-3p的下调和上调可阻断KGN细胞中HCP5沉默和过表达介导的对增殖和凋亡的影响。另外，miR-27a-3p抑制剂显着逆转了通过敲低HCP5调节的IGF-1降低，而miR-27a-3p模拟物则抑制了KGN细胞中过表达HCP5调节的IGF-1升高。此外，我们观察到当用IGF-1 siRNA转染KGN细胞时，由HCP5的强制表达介导的细胞活力增强和凋亡减少可以减轻。