KLF5 promotes esophageal squamous cell cancer through the transcriptional activation of FGFBP1.
Fengyun WangMing LuoYufeng ChengPublished in: Medical oncology (Northwood, London, England) (2023)
Krüpple-like factor 5 (KLF5) is a zinc-finger-containing transcription factor implicated in several human malignancies, but its potential regulatory mechanisms implicated in esophageal squamous cell carcinoma (ESCC) remain elusive. Here, we show that KLF5 is upregulated in ESCC, where its level was significantly associated with tumor differentiation and lymph node metastasis status. Upregulated KLF5 expression promoted the proliferation, migration, and invasion of ESCC cells. Reduced KLF5 showed the opposite effects. Mechanistically, KLF5 exerts its tumor promotion effect by up-regulating fibroblast growth factor binding protein 1 (FGF-BP1) and snail family transcriptional repressor 2 (SNAIL2). KLF5 binds to the promoter regions of FGF-BP1 and transcriptionally activates its expression. Our study indicated that KLF5 could promote esophageal squamous cell cancer proliferation, migration, and invasion by upregulating FGF-BP1/SNAIL2 signaling. Our work suggests that KLF5 might be a proto-oncogene in ESCC and implicated in ESCC metastasis.
Keyphrases
- transcription factor
- squamous cell
- papillary thyroid
- lymph node metastasis
- binding protein
- dna binding
- epithelial mesenchymal transition
- poor prognosis
- squamous cell carcinoma
- gene expression
- induced apoptosis
- dna methylation
- signaling pathway
- endothelial cells
- genome wide identification
- long non coding rna
- endoplasmic reticulum stress
- cell cycle arrest
- cell death