Effects of CREB on migration,invasion,and cell cycle of prostate cancer PC3 cells
10.3872/j.issn.1007-385x.2025.06.004
- VernacularTitle:环磷腺苷效应元件结合蛋白对前列腺癌PC3细胞迁移、侵袭和细胞周期的影响
- Author:
Rui LI
1
;
Liu YANG
1
;
Jiayun LIU
1
Author Information
1. 空军军医大学附属西京医院 全军临床医学检验研究所,陕西 西安 710032
- Publication Type:Journal Article
- Keywords:
prostate cancer;
CRISPR/Cas9;
cyclic adenosine monophosphate responsive element binding protein(CREB)gene;
cell cycle;
migration;
invasion
- From:
Chinese Journal of Cancer Biotherapy
2025;32(6):587-593
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of cyclic adenosine monophosphate response element binding protein(CREB)on the malignant biological behaviors of prostate cancer PC3 cells.Methods:Prostate cancer PC3 cells were routinely cultured.The overexpression control plasmid(vector),CREB overexpression plasmid(CREB-oe),knockdown control sequence(si-NC),and si-CREB sequence were transfected into PC3 cells using transfection reagents,namely vector,CREB-oe,si-NC,and si-CREB groups.Scratch wound healing assay,Transwell chamber assay,and flow cytometry were performed to evaluate cell migration,invasion,and cell cycle distribution,respectively.PC3 cells with CREB knockout were constructed using CRISPR/Cas9 technology,and a xenograft tumor model was employed to evaluate the impact of CREB knockout on tumor growth in vivo.Results:CREB was successfully knocked down or overexpressed in PC3 cells(all P<0.01).CREB overexpression significantly promoted,while its knockdown significantly inhibited the migration and invasion of PC3 cells(all P<0.01).Overexpression of CREB promoted the transition of PC3 cells into the S phase,whereas knockdown of CREB induced G1 phase arrest(all P<0.01).PC3 cells with CREB knockout were successfully constructed,and CREB knockout significantly inhibited the growth of PC3 cell-transplanted tumors(P<0.01).Conclusion:Knockdown or knockout of CREB inhibits migration and invasion of PC3 cells and induces G1 phase arrest,thereby suppressing tumor growth.
