| 刘晓英,沈 鑫,张 静,荣 晅,邓 卓.干扰素诱导的跨膜蛋白1在宫颈鳞癌中的表达及其生物学作用[J].,2021,(1):34-41 |
| 干扰素诱导的跨膜蛋白1在宫颈鳞癌中的表达及其生物学作用 |
| Expression of Interferon-induced Transmembrane Protein 1 in Cervical Squamous Cell Carcinoma and Its Biological Effects |
| 投稿时间：2020-04-27 修订日期：2020-05-23 |
| DOI：10.13241/j.cnki.pmb.2021.01.006 |
| 中文关键词: 干扰素诱导的跨膜蛋白1 宫颈鳞癌 细胞增殖 迁移 侵袭 PTEN/PI3K/AKT信号通路 |
| 英文关键词: Interferon-induced transmembrane protein 1 Cervical squamous cell carcinoma Cell proliferation Migration Invasion PTEN/PI3K/AKT signaling pathway |
| 基金项目:陕西省社会发展科技攻关项目（2016SF-181） |
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| 中文摘要: |
| 摘要 目的：探讨干扰素诱导的跨膜蛋白1（IFITM1）在宫颈鳞癌中的表达及其生物学作用。方法：通过免疫组化、RT-PCR和Western blot检测宫颈鳞癌组织和癌旁组织中IFITM1的表达。使用靶向IFITM1的siRNA（si-IFITM1组）和高表达IFITM1基因的重组pcDNA3.1质粒（pcDNA3.1-si-IFITM1组）转染SiHa细胞下调或上调IFITM1的表达。通过伤口愈合实验、Transwells迁移实验和基质胶侵袭实验检测细胞迁移和侵袭能力。细胞计数试剂盒-8（CCK-8）检测细胞增殖；流式细胞术测定细胞凋亡。Western blot检测PTEN、PI3K和AKT的表达。通过对BALB/c Nude裸鼠接种SiHa细胞来考察IFITM1在体外对肿瘤生长的影响。结果：癌组织中IFITM1的表达水平明显高于癌旁组织（P<0.05）。与对照组比较，si-IFITM1组的迁移和侵袭能力明显增强，而pcDNA3.1-si-IFITM1组明显降低（P<0.05）。细胞转染48 h和72 h后，与对照组比较，si-IFITM1组的细胞增殖明显增强，而pcDNA3.1-si-IFITM1组明显减弱（P<0.05）。与对照组比较，si-IFITM1组的细胞凋亡率明显降低，而pcDNA3.1-si-IFITM1组明显升高（P<0.05）。与对照组比较，si-IFITM1组的PTEN被下调，而PI3K和AKT被上调（P<0.05）；pcDNA3.1-si-IFITM1组的PTEN的被上调，而PI3K和AKT被下调（P<0.05）。与对照组比较，si-IFITM1组裸鼠的肿瘤体积显著增大，而pcDNA3.1-si-IFITM1组显著减小（P<0.05）。结论：IFITM1过表达抑制人宫颈鳞癌细胞SiHa的生长和转移能力，并在体外抑制肿瘤的形成，从而发挥抗癌作用。IFITM1可能通过调控PTEN/PI3K/AKT信号通路发挥抗癌作用。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the expression and biological roles of interferon-induced transmembrane protein 1 (IFITM1) in cervical squamous cell carcinoma. Methods: The expression of IFITM1 in cervical squamous cell carcinoma and paracancerous tissues was detected by immunohistochemistry, RT-PCR and Western blot. The siRNAs targeting IFITM1 (si-IFITM1 group) and recombinant pcDNA3.1 plasmid that highly express IFITM1 gene (pcDNA3.1-si-IFITM1 group) were transfected into SiHa cells to down-regulate or up-regulate IFITM1 expression, respectively. Cell migration and invasion were tested by wound healing experiments, Transwells migration experiments, and matrigel invasion experiments. Cell Counting Kit-8 (CCK-8) was used to detect cell proliferation. Apoptosis was measured by flow cytometry. Western blot was used to detect the expression of PTEN, PI3K and AKT. The effect of IFITM1 on tumor growth in vitro was investigated by inoculating BALB/c Nude nude mice with SiHa cells. Results: The expression level of IFITM1 in cancer tissues was significantly higher than that in paracancerous tissues (P<0.05). Compared with the control group, the migration and invasion capabilities in the si-IFITM1 group were significantly enhanced, while that of the pcDNA3.1-si-IFITM1 group were significantly reduced (P<0.05). At 48 h and 72 h after cell transfection, compared with the control group, the cell proliferation of the si-IFITM1 group was significantly enhanced, while that of the pcDNA3.1-si-IFITM1 group was significantly reduced (P<0.05). Compared with the control group, the apoptosis rate of the si-IFITM1 group was significantly reduced, while that of the pcDNA3.1-si-IFITM1 group was significantly increased (P<0.05). Compared with the control group, PTEN in the si-IFITM1 group was down-regulated, while PI3K and AKT were up-regulated (P<0.05). PTEN in the pcDNA3.1-si-IFITM1 group was up-regulated, while PI3K and AKT were down-regulated (P<0.05). Compared with the control group, the tumor volume of the nude mice in the si-IFITM1 group increased significantly, while that in the pcDNA3.1-si-IFITM1 group decreased significantly (P<0.05). Conclusion: Overexpression of IFITM1 can inhibit the growth and metastasis of human cervical squamous carcinoma cell line SiHa, and inhibit tumor formation in vitro, thereby exerting anti-cancer effect. IFITM1 may play an anti-cancer role by regulating the PTEN/PI3K/AKT signaling pathway. |
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