E2F7-mediated CXCL5 transcription to promote anaplastic thyroid cancer progression
10.12007/j.issn.0258-4646.2024.10.007
- VernacularTitle:E2F7介导CXCL5转录促进未分化甲状腺癌发展
- Author:
Xinghe PAN
1
;
Hongpeng GUO
;
You LI
;
Chenglin SUN
Author Information
1. 沈阳医学院附属中心医院普外一科,沈阳 110024
- Keywords:
E2F7;
anaplastic thyroid cancer;
CXCL5/CXCR2/ERK signaling pathway;
proliferation;
migration and invasion;
tumor growth
- From:
Journal of China Medical University
2024;53(10):907-913
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of transcription factor E2F7 on the proliferation,migration,invasion,and tumor growth of anaplastic thyroid cancer(ATC)cells in vitro and to elucidate the underlying mechanisms.Methods Lentivirus transfection was used for a stable E2F7 knockdown in CAL-62 cells,and real-time PCR was used to detect E2F7 expression in these cells to verify the trans-fection efficiency.CAL-62 cells were divided into sh-NC and sh-E2F7 groups,and cell proliferation was measured using the CCK-8 assay,whereas cell migration and invasion abilities were measured using the Transwell assay.CAL-62 cells were subcutaneously injected into nude mice to observe tumor growth.The EPD website predicted an E2F7 binding site on the CXCL5 promoter,and the dual-lucif-erase reporter gene assay measured the effect of E2F7 knockdown on the luciferase activity of the CXCL5 promoter.The impact of E2F7 knockdown on CXCL5 levels in CAL-62 cells was assessed through real-time PCR and ELISA.Further,CAL-62 cells were divided into sh-E2F7+vector and sh-E2F7+CXCL5 groups to study the effects of CXCL5 overexpression on cell proliferation,migration,invasion,and the CXCR2/ERK signaling pathway following E2F7 knockdown.Results E2F7 knockdown inhibited CAL-62 cell proliferation,migra-tion,and invasion in vitro and tumor growth in vivo.The CXCL5 promoter has an E2F7 binding site,and E2F7 knockdown reduced the luciferase activity of the CXCL5 promoter.CXCL5 overexpression reversed the inhibitory effect of E2F7 knockdown on cell proliferation,migration,invasion,and the CXCR2/ERK signaling pathway in CAL-62 cells.Conclusion E2F7 promotes ATC cell proliferation,migra-tion,invasion,and tumor growth in vitro by activating the CXCL5/CXCR2/ERK signaling pathway mediated by CXCL5 transcription.
