ArticleMolecular medicine reports2018
c‑Jun suppresses the expression of WNT inhibitory factor 1 through transcriptional regulation and interaction with DNA methyltransferase 1 in gallbladder cancer.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Enhancer of Zeste Homolog 2 (EZH2) in Malignant Progression of Gallbladder Carcinoma.Journal of gastrointestinal cancer · 2021Article
- The role of N-cadherin/c-Jun/NDRG1 axis in the progression of prostate cancer.International journal of biological sciences · 2021Article
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9 authors at 2 institutions in 1 country.
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Abstract
WNT inhibitory factor 1 (WIF‑1) is involved in the tumorigenicity and progression of several types of tumor, which has been attributed to aberrant hypermethylation of its promoter. However, the role of WIF‑1 in the pathogenesis of gallbladder cancer (GBC) remains to be fully elucidated, and the data available are insufficient to identify the upstream molecular mechanisms involved. In the present study, the methylation status of the WIF‑1 promoter was investigated using methylation‑specific polymerase chain reaction (PCR) and bisulfate sequencing PCR in GBC cells. Immunohistochemistry, reverse transcription‑quantitative PCR and western blotting were used to analyze the expression of WIF‑1 and c‑Jun. In addition, a co‑immunoprecipitation assay was designed to determine the DNA methyltransferase that was implicated in WIF‑1 methylation. The results revealed that the expression of WIF‑1 was low in GBC, and that this was caused by aberrant DNA hypermethylation. However, there were no significant correlations between the expression of WIF‑1 and certain key clinicopathological characteristics of GCB. Subsequently, a negative correlation was found between the protein expression of c‑Jun and WIF‑1 in 50 GBC specimens using immunohistochemistry. The demethylation and re‑expression of WIF‑1 was observed when the expression of c‑Jun was silenced. Finally, it was found that the knockdown of c‑Jun downregulated the expression of DNA methyltransferase 1 (DNMT1) and that c‑Jun interacted with DNMT1. Taken together, the present study suggested that c‑Jun suppressed the expression of WIF‑1 through transcriptional regulation and interaction with DNMT1 in GBC. These findings provide an alternative pathogenesis of GBC, which may be promising as a novel reference for early diagnosis or future treatment.
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