English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

The Krüppel-associated box zinc-finger protein 545 (ZNF545) was recently identified as a tumor suppressor in esophageal squamous cell carcinoma (ESCC). However, the role of ZNF545 in the tumorigenesis of esophageal cancer cells expressing loss-of-function mutant p53 has not been elucidated. In the present study, the role of ZNF545 in esophageal tumors and the p53-mutant ESCC cell line, KYSE150, was investigated. ZNF545 mRNA was significantly downregulated in tumors when compared with adjacent normal tissues. Methylated ZNF545 was detected in 76.6% of tumor tissues compared with 28.1% of adjacent normal tissues. Combined pharmacological treatment of KYSE150 cells with a demethylating reagent and deacetylase inhibitor restored the expression of ZNF545. Ectopic expression of ZNF545 activated p53 transcription and upregulated the protein expression levels of pivotal effectors p21 and Bax, which are associated with cell proliferation and apoptosis, respectively, in p53-mutant KYSE150 cells; while suppressing colony formation and inducing apoptosis. ZNF545 was therefore proposed as a potential tumor suppressor responsible for inhibiting the growth of p53-mutant ESCC cell lines. In addition, tumor-specific methylation of ZNF545 may represent an epigenetic diagnostic biomarker and a therapeutic target in patients with esophageal cancer.

Methylation‑regulated ZNF545 inhibits growth of the p53‑mutant KYSE150 cell line by inducing p21 and Bax