4.7 Article

TRIM47 promotes malignant progression of renal cell carcinoma by degrading P53 through ubiquitination

期刊

CANCER CELL INTERNATIONAL
卷 21, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12935-021-01831-0

关键词

Renal cell carcinoma; E3 ubiquitin ligase; Proliferation; P53; TRIM47

类别

资金

  1. National Natural Science Foundation of China [81772747, 81974391, 82072806]
  2. Program of Shanghai Academic/Technology Research Leader [19XD1405100]
  3. Clinical Research Plan of SHDC [SHDC2020CR4025]
  4. Shanghai Rising Stars of Medical Talent Youth Development Program: Outstanding Youth Medical Talents
  5. Youth Medical Talents -Specialist Program
  6. Top-level Clinical Discipline Project of Shanghai Pudong [PWYgf2018-03]
  7. Shanghai Key Medical Specialties Project [ZK2019A09]
  8. Shanghai Municipal Commission of Health and Family Planning [20204Y0042]
  9. Technology Project of Jiading District Health System [2019-QN-03]

向作者/读者索取更多资源

This study demonstrated the crucial role of TRIM47 in promoting malignant biological behavior in renal cell carcinoma, by interacting with P53 protein to increase its ubiquitination and degradation; The TRIM47-P53 axis might be a potential therapeutic target for RCC progression.
Background Renal cell carcinoma (RCC) is one of the most common malignant tumors originating from the renal parenchymal urinary epithelial system. Tripartite motif 47 (TRIM47) is a member of the TRIM family proteins, which has E3 ligase activity and has been demonstrated to be involved in the occurrence and prognosis of many tumors. The main purpose of this study is to explore the role and potential mechanism of TRIM47 in promoting malignant biological behavior of RCC. Materials and methods TRIM47 mRNA and protein levels in human renal cancer and paired normal adjacent tissues were detected by qRT-PCR and Western blot. The effects of TRIM47 knockdown and overexpression in renal cell carcinoma cells on cell proliferation, invasion and xenograft tumor growth in nude mice were analyzed. The molecular mechanism was explored by mass spectrometric exploration,Western blot and immunoprecipitation assays. Results TRIM47 promoted RCC cell proliferation in vitro and in vivo as an oncogene. Mechanistically, TRIM47 exerted an E3 ligase activity by interacting with P53 protein to increase its ubiquitination and degradation, which further promoted the malignant biological behavior of RCC. Conclusions Our study demonstrated that the TRIM47-P53 axis played a functional role in RCC progression and suggested a potential therapeutic target for RCC.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据