E2F1 promotes cell migration in hepatocellular carcinoma via FNDC3B

被引:1
作者
Hua, Kate [1 ]
Wu, Chen-Tang [1 ]
Lin, Chin-Hui [1 ]
Chen, Chian-Feng [1 ]
机构
[1] Natl Yang Ming Chiao Tung Univ, Canc Progress Res Ctr, 155 Sec 2,Linong St, Taipei, Taiwan
来源
FEBS OPEN BIO | 2024年 / 14卷 / 04期
关键词
ChIP; ddPCR; E2F1; FNDC3B; hepatocellular carcinoma; transcription factor; EPITHELIAL-MESENCHYMAL TRANSITION; CANCER; PROLIFERATION; CIS;
D O I
10.1002/2211-5463.13783
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
FNDC3B (fibronectin type III domain containing 3B) is highly expressed in hepatocellular carcinoma (HCC) and other cancer types, and fusion genes involving FNDC3B have been identified in HCC and leukemia. Growing evidence suggests the significance of FNDC3B in tumorigenesis, particularly in cell migration and tumor metastasis. However, its regulatory mechanisms remain elusive. In this study, we employed bioinformatic, gene regulation, and protein-DNA interaction screening to investigate the transcription factors (TFs) involved in regulating FNDC3B. Initially, 338 candidate TFs were selected based on previous chromatin immunoprecipitation (ChIP)-seq experiments available in public domain databases. Through TF knockdown screening and ChIP coupled with Droplet Digital PCR assays, we identified that E2F1 (E2F transcription factor 1) is crucial for the activation of FNDC3B. Overexpression or knockdown of E2F1 significantly impacts the expression of FNDC3B. In conclusion, our study elucidated the mechanistic link between FNDC3B and E2F1. These findings contribute to a better understanding of FNDC3B in tumorigenesis and provide insights into potential therapeutic targets for cancer treatment.
引用
收藏
页码:687 / 694
页数:8
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