May 28, 2020

Jab1 promotes gastric cancer tumorigenesis via non-ubiquitin proteasomal degradation of p14ARF

Gastric Cancer : Official Journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association
Lin WangDong-Sheng Pei

Abstract

Jab1 has been reported to regulate various proteins in signal transduction pathways and be implicated in carcinogenesis or tumor progression. However, the precise role and molecular mechanism of Jab1 in gastric tumorigenesis have not yet been fully elucidated. Jab1 staining in gastric cancer tissues and paired non-cancerous tissues was measured using tissue microarray (TMA) technology. The impact of Jab1 on tumor growth in vivo was analyzed using xenotransplantation experiments in Balb/c mice. The expression of Jab1 and p14ARF in gastric cancer cells was analyzed by western blot and confocal immunofluorescence. CCK-8 and cell cycle experiment were used to evaluate the cell proliferation. Ubiquitination assay was performed to validate whether ubiquitination is involved in Jab1-mediated p14ARF degradation. The expression level of protein p14ARF was inversely correlated with the protein level of Jab1. Then, we investigated the mechanism that how Jab1 induced p14ARF depletion. Mechanistic studies showed that Jab1 induced ubiquitin-independent proteasomal p14ARF degradation in gastric cancer cells. Our data demonstrated that Jab1 protein was a vital upstream negative modulation factor of p14ARF, and Jab1 could promote cell prolifera...Continue Reading

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Mentioned in this Paper

COPS5 protein, human
Mice, Inbred BALB C
Molecular_function
Microarray Analysis
Protein Expression
Tumor Progression
Xenograft Procedure
Gene Silencing
Microscopy, Confocal
Ubiquitination

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