학술논문

Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53
Document Type
Academic Journal
Source
Oncology Letters. January, 2021, Vol. 21 Issue 1, p1e, p13 p.
Subject
United States
China
Language
English
ISSN
1792-1074
Abstract
Human esophageal cancer (hESC) cell motility adopts various modes, resulting in hESC progression and poor survival. However, how tripartite motif 59 (TRIM59), as the ubiquitination machinery, participates in hESC metastasis is not completely understood. The results indicated that TRIM59 was aberrantly upregulated in hESC tissues compared with adjacent healthy esophageal tissues, which was associated with poor survival and advanced TNM state among patients with hESC. Moreover, patients with hESC with higher TRIM59 expression displayed undetectable p53 expression, which contributed to enhanced progression and motility of hESC. At the molecular level, TRIM59 was indicated to be an E3 putative ubiquitin ligase that targeted the p53 protein, leading to increased degradation of p53, which resulted in decreased chemosensitivity to cisplatin. TRIM59 knockdown reduced TRIM59 expression, increased p53 protein expression, and decreased hESC cell viability, clone formation and migration compared with the small interfering RNA negative control (siNC) group. Furthermore, hESC cell lines were more sensitive to cisplatin in the TRIM59-knockdown group compared with the siNC group. The results indicated a relationship between TRIM59, p53 and the chemosensitivity of cisplatin. The present study suggested that TRIM59 may serve as a promising prognostic indicator for patients with hESC. Key words: esophageal cancer, tripartite motif 59, cisplatin, p53, chemosensitivity
Introduction Tripartite motif 59 (TRIM59) is a member of the TRIM family, which is characterized by an N-terminal really interesting new gene (RING)-finger domain, followed by two zinc-finger domains, B2 [...]