Department of Gynaecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Institute of Biological Medicine, Wuhan University of Science and Technology, Wuhan, Hubei 430065, China.
Chem Biol Interact. 2018 Apr 25;286:106-110. doi: 10.1016/j.cbi.2018.03.010. Epub 2018 Mar 20.
Homeobox (HOX) transcript antisense RNA (HOTAIR) is a long intergenic non-coding RNA (lncRNA) that has been reported to be highly upregulated in several types of cancers. However, the role of HOTAIR in human cervical cancer is still unclear. We therefore investigated the expression and probable function of HOTAIR in cervical cancer cells. The expression of HOTAIR was examined in (HeLa, CaSki, ME-180, HT-3) and Human Cervical Epithelial Cells (HCerEpiC) by qRT-PCR. Transfection of si-NC, si-HOTAIR or si-STAT3 was carried out with the help of Lipofectamine 2000. The cell viability was assessed by CCK-8 assay. The cell migration and invasion was examined by wound healing and Boyden chamber assays. Protein expression was determined by western blotting. Our results showed that expression of HOTAIR was significantly upregulated in cervical cancer cells and inhibition of the expression of HOTAIR in HeLa cervical cancer cells resulted in suppression of cell proliferation, migration and invasion. Further, analysis of the promoter of HOTAIR, revealed that STAT3 could potentially regulate the activity of the HOTAIR in cervical cancer cells and inhibition of STAT3 had similar effects on the proliferation, migration and invasion of the cervical cancer cells as that of HOTAIR. Further, the suppression of STAT3 expression was associated with concomitant downregulation of IncRNA HOTAIR as indicated by the qRT-PCR. To unveil if STAT3 and HOTAIR have synergistic effects on the cell migration and invasion, si-STAT3 and si-HOTAIR were co-transformed into cervical HeLa cancer cells and it was observed that STAT3 and HOTAIR could synergistically inhibit the proliferation, migration and invasion of the cervical cancer cells. Taken together we conclude that HOTAIR and STAT3 synergistically regulate the proliferation, migration and invasion of cervical cancer cells.
同源盒（HOX）转录反义 RNA（HOTAIR）是一种长的基因间非编码 RNA（lncRNA），已被报道在几种类型的癌症中高度上调。然而，HOTAIR 在人宫颈癌中的作用尚不清楚。因此，我们研究了 HOTAIR 在宫颈癌细胞中的表达和可能的功能。通过 qRT-PCR 检测（HeLa、CaSki、ME-180、HT-3）和人宫颈上皮细胞（HCerEpiC）中 HOTAIR 的表达。借助 Lipofectamine 2000 转染 si-NC、si-HOTAIR 或 si-STAT3。通过 CCK-8 测定评估细胞活力。通过划痕愈合和 Boyden 室测定检测细胞迁移和侵袭。通过 Western blot 测定测定蛋白表达。我们的结果表明，HOTAIR 在宫颈癌细胞中的表达明显上调，抑制 HeLa 宫颈癌细胞中 HOTAIR 的表达导致细胞增殖、迁移和侵袭受到抑制。进一步分析 HOTAIR 的启动子，发现 STAT3 可能潜在地调节宫颈癌细胞中 HOTAIR 的活性，抑制 STAT3 对宫颈癌细胞的增殖、迁移和侵袭具有与 HOTAIR 相似的作用。此外，如 qRT-PCR 所示，STAT3 表达的抑制与 IncRNA HOTAIR 的伴随下调相关。为了揭示 STAT3 和 HOTAIR 是否对细胞迁移和侵袭具有协同作用，将 si-STAT3 和 si-HOTAIR 共转染入宫颈 HeLa 癌细胞，并观察到 STAT3 和 HOTAIR 可协同抑制宫颈癌细胞的增殖、迁移和侵袭。总之，我们得出结论，HOTAIR 和 STAT3 协同调节宫颈癌细胞的增殖、迁移和侵袭。
