Epigenomic characterization of a p53-regulated 3p22.2 tumor suppressor that inhibits STAT3 phosphorylation via protein docking and is frequently methylated in esophageal and other carcinomas

Theranostics
Lili LiQian Tao

Abstract

Rationale: Oncogenic STAT3 signaling activation and 3p22-21.3 locus alteration are common in multiple tumors, especially carcinomas of the nasopharynx, esophagus and lung. Whether these two events are linked remains unclear. Our CpG methylome analysis identified a 3p22.2 gene, DLEC1, as a methylated target in esophageal squamous cell (ESCC), nasopharyngeal (NPC) and lung carcinomas. Thus, we further characterized its epigenetic abnormalities and functions. Methods: CpG methylomes were established by methylated DNA immunoprecipitation. Promoter methylation was analyzed by methylation-specific PCR and bisulfite genomic sequencing. DLEC1 expression and clinical significance were analyzed using TCGA database. DLEC1 functions were analyzed by transfections followed by various cell biology assays. Protein-protein interaction was assessed by docking, Western blot and immunoprecipitation analyses. Results: We defined the DLEC1 promoter within a CpG island and p53-regulated. DLEC1 was frequently downregulated in ESCC, lung and NPC cell lines and primary tumors, but was readily expressed in normal tissues and immortalized normal epithelial cells, with mutations rarely detected. DLEC1 methylation was frequently detected in ESCC tumors and...Continue Reading

Citations

Jan 9, 2019·Frontiers in Neuroscience·Boris Rebolledo-Jaramillo, Annemarie Ziegler
Nov 7, 2019·Biomarker Research·Mingzhou GuoJames G Herman
Oct 24, 2020·Signal Transduction and Targeted Therapy·Yuanbo KangLei Wang
Nov 5, 2020·Scientific Reports·Yu OkitsuKeiichiro Yogo

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Datasets Mentioned

BETA
AY789462
AY789463
AY789464
AB020522

Methods Mentioned

BETA
immunoprecipitation
PCR
ChIP
confocal microscopy
co-immunoprecipitation
co-IP
histone acetylation

Software Mentioned

MotifSearch
ZDOCK
RCSB
R
TFSEARCH

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