2. Academic Validation
  3. NSD1 promotes esophageal cancer tumorigenesis via HIF1α signaling

NSD1 promotes esophageal cancer tumorigenesis via HIF1α signaling

  • Cell Biol Toxicol. 2022 Dec 16. doi: 10.1007/s10565-022-09786-2.
Feng He 1,  Hang Xiao 1,  Yixin Cai 1,  Ni Zhang 2
Affiliations

Affiliations

  • 1 Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, China.
  • 2 Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, China. [email protected].
PMID: 36522543 DOI: 10.1007/s10565-022-09786-2
Abstract

Unlike angiogenesis in normal tissues, tumor angiogenesis is typically dysregulated, during which the HIF1/VEGFA signaling pathway plays a pivotal role. Solid tumors generate immature vessels, which promote tumor progression and treatment resistance. NSD1 can di-methylate histone 3 lysine 36 and regulate transcription factors binding to the promoters of various genes. However, the role of NSD1 in tumorigenesis remains elusive. Here, we evaluated the relationship between NSD1 signaling and HIF1 signaling. It was found that NSD1 transcriptionally regulates HIF1α expression by recruiting STAT3 molecule into the HIF1α promoter. In vivo xenograft experiments further confirmed that HIF1α and STAT3 maintenance is essential for NSD1-mediated tumor progression and angiogenesis. Therefore, the NSD1/STAT3/HIF1α signaling pathway may be a novel and effective treatment target for ESCA.

Keywords

Angiogenesis; HIF1; NSD1; STAT3.

Figures
Products