Department of Obstetrics, Affiliated Hospital of Weifang Medical University, Weifang, China.
Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9282-9289. doi: 10.26355/eurrev_202009_23010.
This study was designed to investigate the specific mechanism through which long non-coding RNA (lncRNA) SNHG17 promotes the proliferative capacity and invasiveness of ovarian tumor cells.
Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) detected the expressions of SNHG17 and FOXA1 in 30 pairs of ovarian cancer tissue specimens and corresponding adjacent ones. Meanwhile, in ovarian cancer cell lines (A2780, OVCAR3, SKOV3, CAOV3) and normal ovarian epithelial cell line (IOSE80), SNHG17 and FOXA1 mRNA levels were also examined. In in vitro experiment, si-SNHG17, si-FOXA1, and their corresponding negative controls were transfected into ovarian cancer cell lines, respectively. After that, Cell Counting Kit-8 (CCK-8) and plate cloning experiments were carried out to examine cell proliferation ability, while transwell assay was performed for cell invasiveness detection. Lastly, the interplay between SNHG17 and FOXA1 was further assessed via qRT-PCR and Western blot.
qRT-PCR results indicated that SNHG17 expression was remarkably enhanced in ovarian cancer tissue samples compared with that in adjacent ones. In addition, ovarian cancer cells also contained higher expression of SNHG17 than the normal ovarian epithelial cells. However, down-regulating SNHG17 attenuated the cell proliferation and invasive ability. At the same time, compared with that in adjacent tissue samples, FOXA1 also showed a higher expression in ovarian cancer tissues, which was positively correlated with SNHG17. Silencing SNHG17 markedly downregulated FOXA1 expression at both mRNA and protein levels. Furthermore, downregulation of FOXA1 expression was found to be able to inhibit cell proliferation and invasion as well.
LncRNA SNHG17 can promote ovarian tumor cell proliferative ability and invasiveness by upregulating FOXA1, and serve as a potential therapeutic target for ovarian cancer.
本研究旨在探讨长链非编码 RNA（lncRNA）SNHG17 促进卵巢肿瘤细胞增殖和侵袭能力的具体机制。
采用实时定量聚合酶链反应（qRT-PCR）检测 30 对卵巢癌组织标本及其相应癌旁组织中 SNHG17 和 FOXA1 的表达情况。同时，在卵巢癌细胞系（A2780、OVCAR3、SKOV3、CAOV3）和正常卵巢上皮细胞系（IOSE80）中检测 SNHG17 和 FOXA1 mRNA 水平。在体外实验中，分别将 si-SNHG17、si-FOXA1 及其相应的阴性对照转染至卵巢癌细胞系中，然后进行细胞计数试剂盒-8（CCK-8）和平板克隆实验以检测细胞增殖能力，以及 Transwell 实验检测细胞侵袭能力。最后，通过 qRT-PCR 和 Western blot 进一步评估 SNHG17 和 FOXA1 之间的相互作用。
qRT-PCR 结果表明，与癌旁组织相比，卵巢癌组织中 SNHG17 的表达显著升高。此外，卵巢癌细胞中 SNHG17 的表达也高于正常卵巢上皮细胞。然而，下调 SNHG17 可减弱细胞增殖和侵袭能力。同时，与癌旁组织相比，FOXA1 在卵巢癌组织中也表现出较高的表达，且与 SNHG17 呈正相关。沉默 SNHG17 可显著下调 SNHG17 及其蛋白水平的 FOXA1 表达。此外，下调 FOXA1 表达也可抑制细胞增殖和侵袭。
lncRNA SNHG17 通过上调 FOXA1 促进卵巢肿瘤细胞的增殖能力和侵袭能力，可作为卵巢癌的潜在治疗靶点。
