Journal of International Oncology ›› 2022, Vol. 49 ›› Issue (3): 129-133.doi: 10.3760/cma.j.cn371439-20210917-00022

• Original Articles •     Next Articles

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)

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