| 阿木提江·马合木提,买热帕提·艾尔凯西,郑坚江,迪里夏提·阿里木,陈 雄.MiR-194-5p靶向调控HMGA2抑制TGF-β1诱导的胰腺癌EMT的作用[J].现代生物医学进展英文版,2024,(13):2440-2444. |
| MiR-194-5p靶向调控HMGA2抑制TGF-β1诱导的胰腺癌EMT的作用 |
| MiR-194-5p Targeted Regulation of HMGA2 to Inhibit EMT Induced by TGF-β1 in Pancreatic Cancer |
| Received:December 27, 2023 Revised:January 20, 2024 |
| DOI：10.13241/j.cnki.pmb.2024.13.007 |
| 中文关键词: 胰腺癌 上皮－间质转化 转化生长因子-β1 高迁移率族蛋白2 miR-194-5p |
| 英文关键词: Pancreatic cancer Epithelial mesenchymal transition Transforming growth factor-β1 High mobility group A2 MiR-194-5p |
| 基金项目:新疆少数民族科技人才特殊培养计划科研项目（2021D03019） |
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| 中文摘要: |
| 摘要 目的：研究miR-194-5p靶向调控高迁移率族蛋白2（HMGA2）表达，进而抑制转化生长因子（TGF）-β1诱导的胰腺癌细胞上皮－间质转化（EMT）的相关分子机制。方法：将人胰腺癌细胞系Bx Pc-3分为四组，分别为对照组、处理组、Sh-miR-194-5p组和Sh-NC组，除了对照组，其他三组均在体外采用TGF-β1诱导培养72 h，分别构建miR-194-5p沉默质粒（Sh-miR-194-5p）和对照质粒（Sh-NC）在TGF-β1诱导培养前2 h转染细胞。倒置显微镜观察细胞形态，qRT-PCR法检测miR-194-5p，Western blot法检测HMGA2以及EMT标志物（E-cadherin、Vimentin和N-cadherin）蛋白，Transwell实验检测细胞侵袭。结果：与对照组相比，处理组细胞形态为长梭形，出现 EMT 特征性形态；miR-194-5p、HMGA2、Vimentin和N-cadherin表达量明显升高，而E-cadherin表达量明显下降，侵袭细胞数目减少（P＜0.05）。与处理组和Sh-NC组相比，Sh-miR-194-5p组细胞形态变化明显减少，但仍多于对照组，miR-194-5p、HMGA2、Vimentin和N-cadherin表达量明显下降，而E-cadherin表达量明显升高，侵袭细胞数目增多（P＜0.05），与对照组相比差异仍有统计学意义（P＜0.05）。结论：人胰腺癌细胞可高表达miR-194-5p，通过靶向调控HMGA2表达进而部分程度上抑制了TGF-β1诱导的细胞EMT变化，为疾病发生机制以及临床干预提供了新型靶点。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the targeted regulation of high mobility group A2 (HMGA2) expression by miR-194-5p, thereby inhibiting epithelial mesenchymal transformation (EMT) induced by transforming growth factor (TGF)- β 1 in pancreatic cancer cells. Methods: Human pancreatic cancer cell line BxPc-3 was divided into four groups: control group, treatment group, Sh-miR-194-5p group and Sh-NC group. Except the control group, the other three groups were treated with TGF- β1 in vitro to induce and cultivate for 72 h, what's more, miR-194-5p silencing plasmid (Sh-miR-194-5p) and control plasmid (Sh-NC) were constructed to transfect cells 2 h before TGF- β1 induced culture. The morphological changes of cells were observed under inverted microscope, qRT-PCR was to detect miR-194-5p, Western blot was to detect protein expression of HMGA2 and EMT markers (E-cadherin, Vimentin, and N-cadherin), Transwell assay was to detect the invasiveness of cells. Results: Compared with control group, the cell morphology of the treatment group changed to a long spindle shape, exhibiting characteristic morphological changes of EMT; the expression levels of miR-194-5p, HMGA2, Vimentin, and N-cadherin were significantly higher, while the expression level of E-cadherin was significantly lower, the number of invasive cells was less, too(P<0.05). Compared with the treatment group and Sh-NC group, the morphological changes of cells in the Sh-miR-194-5p group were significantly less, but still more than the control group, the expression levels of miR-194-5p, HMGA2, Vimentin, and N-cadherin were significantly lower, but the expression level of E-cadherin was significantly more and number of invasive cells was more, too(P<0.05), the differences between the Sh-miR-194-5p group and the control group were still statistically significant (P<0.05). Conclusion: Human pancreatic cancer cells may overexpress miR-194-5p, which partially inhibits cell EMT changes induced by TGF-β1 via targetly regulating HMGA2 expression. It can provide novel targets for disease pathogenesis and clinical intervention. |
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