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论著·基础研究 | 更新时间:2026-07-13
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敲低DSG2对鼻咽癌细胞增殖、侵袭、迁移及上皮-间质转化的影响
Effect of DSG2 knockdown on proliferation, invasion, migration, and epithelial⁃mesenchymal transition of nasopharyngeal carcinoma cells

广西医学 页码:877-884

作者机构:颜致宇,硕士,住院医师,研究方向为肿瘤学。

基金信息:广西科技计划项目(桂科AB23026020);广西区域性高发肿瘤早期防治研究教育部重点实验室自主研究项目(GKE⁃ZZ202306)

DOI:10.11675/j.issn.0253⁃4304.2026.06.16

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目的 探讨敲低桥粒芯糖蛋白2(DSG2)对鼻咽癌细胞增殖、侵袭、迁移及上皮-间质转化(EMT)的影响。方法 常规培养鼻咽癌细胞CNE⁃2R和鼻咽正常上皮细胞NP69,将CNE⁃2R细胞分为阴性对照组(NC组,转染空载体慢病毒)和沉默DSG2组(shDSG2组,转染DSG2沉默慢病毒)。通过RT⁃qPCR和Western blot检测CNE⁃2R细胞、NP69细胞,以及NC组与shDSG2组CNE⁃2R细胞中DSG2的mRNA和蛋白表达水平。分别采用细胞增殖⁃毒性检测实验、平板克隆实验、EdU实验、划痕实验及Transwell实验检测并比较NC组和shDSG2组CNE⁃2R细胞的增殖能力、克隆形成能力、增殖率、迁移能力和侵袭能力,采用Western blot检测并比较NC组和shDSG2组CNE⁃2R细胞β⁃连环蛋白、E⁃钙黏蛋白、N⁃钙黏蛋白和波形蛋白的表达水平。结果 CNE⁃2R细胞中DSG2的mRNA和蛋白表达水平较NP69细胞升高(P<0.05);与NC组相比,shDSG2组CNE⁃2R细胞DSG2的mRNA和蛋白表达水平降低(P<0.05)。干预第2、3、4、5天,shDSG2组CNE⁃2R细胞的OD值低于NC组(P<0.05);shDSG2组CNE⁃2R细胞的增殖率、迁移率、细胞克隆团数、迁移和侵袭的细胞数低于或少于NC组(P<0.05)。相较于NC组,shDSG2组CNE⁃2R细胞的E⁃钙黏蛋白表达水平升高,而β⁃连环蛋白、N⁃钙黏蛋白和波形蛋白表达水平降低(P<0.05)。结论 DSG2在鼻咽癌CNE⁃2R细胞中高表达,沉默DSG2能够抑制CNE⁃2R细胞的增殖、迁移和侵袭能力,以及EMT进程。

Objective To investigate the effect of desmoglein 2 (DSG2) knockdown on proliferation, invasion, migration, and epithelial⁃mesenchymal transition (EMT) of nasopharyngeal carcinoma cells. Methods Nasopharyngeal carcinoma CNE‑2R cells and normal nasopharyngeal epithelial NP69 cells were routinely cultured. CNE‑2R cells were divided into negative control group (NC group, transfected with empty vector lentivirus) and DSG2‑silenced group (shDSG2 group, transfected with DSG2‑silenced lentivirus). RT‑qPCR and Western blot were used to detect DSG2 mRNA and protein expressions in CNE‑2R cells, NP69 cells, and CNE‑2R cells from the NC and shDSG2 groups. CNE⁃2R cells proliferation, colony formation, proliferation rate, migration, and invasion were detected and compared between the NC and shDSG2 groups using cell proliferation‑toxicity assay, plate colony formation assay, EdU assay, wound healing assay, and Transwell assay, respectively. Western blot was performed to detect and compare the expressions of β‑catenin, E‑cadherin, N‑cadherin, and vimentin in CNE‑2R cells between the two groups. Results  DSG2 mRNA and protein expressions were elevated in CNE‑2R cells than in NP69 cells (P<0.05). Compared with the NC group, the shDSG2 group showed reduced DSG2 mRNA and protein expressions in CNE⁃2R cells (P<0.05). On days 2, 3, 4, and 5 of the intervention, the OD values of CNE‑2R cells in the shDSG2 group were lower than those in the NC group (P<0.05). The proliferation rate, migration rate, number of colony‑forming units, and numbers of migrating and invading cells of CNE‑2R cells were lower or less in the shDSG2 group compared with the NC group (P<0.05). Relative to the NC group, the shDSG2 group exhibited increased E‑cadherin expression and decreased expressions of β‑catenin, N‑cadherin, and vimentin in CNE⁃2R cells (P<0.05). Conclusion DSG2 is highly expressed in nasopharygeal carcinoma CNE‑2R cells. Silencing DSG2 suppresses the proliferation, migration, and invasion of CNE‑2R cells and inhibits the EMT process.  

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