国际肿瘤学杂志

国际肿瘤学杂志 ›› 2022, Vol. 49 ›› Issue (3): 129-133.doi: 10.3760/cma.j.cn371439-20210917-00022

• 论著 •    下一篇

沉默PSIP1基因对口腔鳞状细胞癌细胞迁移及侵袭的影响

石雨, 陈曦, 许梦琪, 张滢滢, 冀洪海(), 蒋英英()   

  1. 潍坊医学院口腔医学院,潍坊 261053
  • 收稿日期:2021-09-17 修回日期:2021-11-17 出版日期:2022-03-08 发布日期:2022-03-22
  • 通讯作者: 冀洪海,蒋英英 E-mail:sdwf_ji@163.com;yingying820814@163.com
  • 基金资助:
    山东省自然科学基金(ZR2020MH192);山东省医药卫生科技发展计划(2018WS052);潍坊医学院大学生创新创业训练计划(X2021335);潍坊医学院大学生创新创业训练计划(X2021340)

Effects of PSIP1 gene silencing on migration and invasion of oral squamous cell carcinoma cells

Shi Yu, Chen Xi, Xu Mengqi, Zhang Yingying, Ji Honghai(), Jiang Yingying()   

  1. School of Stomatology, Weifang Medical University, Weifang 261053, China
  • Received:2021-09-17 Revised:2021-11-17 Online:2022-03-08 Published:2022-03-22
  • Contact: Ji Honghai,Jiang Yingying E-mail:sdwf_ji@163.com;yingying820814@163.com
  • Supported by:
    Natural Science Foundation of Shandong Province of China(ZR2020MH192);Medical and Health Science and Technology Development Plan of Shandong Province of China(2018WS052);Students' Innovation and Entrepreneurship Training Program of Weifang Medical University(X2021335);Students' Innovation and Entrepreneurship Training Program of Weifang Medical University(X2021340)

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摘要：

目的 探讨沉默人PC4和SFRS1互动蛋白1(PSIP1)基因在口腔鳞状细胞癌细胞中的表达以及沉默PSIP1对口腔鳞状细胞癌细胞迁移及侵袭能力的影响,并初步探究其机制。方法 采用RNA干扰技术沉默口腔鳞状细胞癌HN30细胞中PSIP1的表达,将细胞分为si-NC组(转染siRNA-NC)和si-PSIP1组(转染siRNA-PSIP1)。采用荧光实时定量PCR检测PSIP1的表达水平;细胞划痕实验和Transwell小室侵袭实验分别检测细胞迁移及侵袭能力;蛋白质印迹法检测两组HN30细胞内上皮间质转化(EMT)相关蛋白的表达情况。结果 PSIP1在si-NC组、si-PSIP1组HN30细胞中的相对表达量分别为1.00±0.00、0.21±0.06,差异具有统计学意义(t=22.30,P=0.002)。si-NC组、si-PSIP1组HN30细胞12 h的划痕愈合率分别为(48.21±4.66)%、(42.05±11.74)%,差异无统计学意义(t=1.46,P=0.173);24 h的划痕愈合率分别为(86.61±6.06)%、(67.76±3.62)%,差异具有统计学意义(t=8.01,P<0.001);两组细胞穿膜数目分别为(91.00±7.05)个、(23.34±4.98)个,差异具有统计学意义(t=19.20,P<0.001);与si-NC组相比,si-PSIP1组HN30细胞的迁移能力及侵袭能力均显著下降(均P<0.001)。si-NC组、si-PSIP1组HN30细胞中上皮钙黏素的相对表达量分别为1.06±0.02、1.43±0.13,差异具有统计学意义(t=-4.94,P=0.036);神经钙黏素的相对表达量分别为1.00±0.04、0.57±0.14,差异具有统计学意义(t=5.03,P=0.007);与si-NC组相比,si-PSIP1组HN30细胞的上皮钙黏素蛋白表达上调,神经钙黏素蛋白表达下调。结论 沉默PSIP1可显著抑制HN30细胞的迁移及侵袭能力,其作用机制可能与PSIP1对口腔鳞状细胞癌EMT途径的影响有关。

关键词: 口腔肿瘤, 细胞运动, 侵袭, PSIP1

Abstract:

Objective To investigate the expression of PC4 and SFRS1 interacting protein 1 (PSIP1) in oral squamous cell carcinoma cells and the effects of PSIP1 silencing on the migration and invasion of oral squamous cell carcinoma cells, and to preliminarily explore its mechanism. Methods The PSIP1 gene of oral squamous cell carcinoma cell line HN30 was silenced by RNA interference technique. HN30 cells were divided into si-NC group (transfected with siRNA-NC) and si-PSIP1 group (transfected with siRNA-PSIP1). Quantitative real-time PCR was used to detect the expression of PSIP1 mRNA. Scratch test and Transwell invasion test were used to detect the migration and invasion abilities of HN30 cells, and Western blotting was used to detect the expression levels of epithelial-mesenchymal transformation (EMT) related proteins in HN30 cells of the two groups. Results The relative expression levels of PSIP1 of HN30 cells in the si-NC group and si-PSIP1 group were 1.00±0.00 and 0.21±0.06 respectively, with a statistically significant difference (t=22.30, P=0.002). The scratch healing rates of the si-NC group and si-PSIP1 were (48.21±4.66)% and (42.05±11.74)% at 12 h respectively, with no statistically significant difference (t=1.46, P=0.173), and the scratch healing rates of the two groups were (86.61±6.06)% and (67.76±3.62)% at 24 h respectively, with a statistically significant difference (t=8.01, P<0.001). The invasion numbers of HN30 cells in the si-NC group and si-PSIP1 group were 91.00±7.05 and 23.34±4.98, and there was a statistically significantly difference (t=19.20, P<0.001). Compared with the si-NC group, the migration and invasion abilities of HN30 cells in the si-PSIP1 group decreased significantly (all P<0.001). The expression levels of E-cadherin of the si-NC group and si-PSIP1 group were 1.06±0.02 and 1.43±0.13 respectively, with a statistically significant difference (t=-4.94, P=0.036), and the expression levels of N-cadherin were 1.00±0.04 and 0.57±0.14 respectively, with a statistically significant difference (t=5.03, P=0.007). Compared with the si-NC group, the expression level of E-cadherin in the si-PSIP1 group increased, while the expression level of N-cadherin decreased. Conclusion Silencing the expression of PSIP1 can significantly inhibit the migration and invasion of HN30 cells, and the mechanism may be related to the effect of PSIP1 on the EMT pathway of oral squamous cell carcinoma.

Key words: Oral neoplasms, Cell movement, Invasion, PSIP1