Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53

Liu,Rongfeng; Li,Hongchen; Xu,Yanzhao; Li,Xing; Guo,Xiaojin; Shi,Jian; Cui,Yanzhi; Wang,Zhiyu; Liu,Junfeng

doi:10.3892/ol.2020.12267

Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53

Authors:
- Rongfeng Liu
- Hongchen Li
- Yanzhao Xu
- Xing Li
- Xiaojin Guo
- Jian Shi
- Yanzhi Cui
- Zhiyu Wang
- Junfeng Liu
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Affiliations: Department of Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China, Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China, Department of Thoracic Surgery, Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China, Department of Immuno‑Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China, Third Department of Thoracic Surgery, Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China
Published online on: November 3, 2020 https://doi.org/10.3892/ol.2020.12267
Article Number: 6
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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.

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