SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer

Ming-Yan Shi; Yarong Wang; Ying Shi; Ruofei Tian; Xiaohong Chen; Hai Zhang; Ke Wang; Ruo Chen

doi:10.1016/j.gendis.2023.02.015

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SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer

Full-length article | 更新时间：2024-02-04

- SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer
- SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer
- Genes & Diseases 2024年11卷第2期
- 作者机构：
  
  National Translational Science Center for Molecular Medicine & Department of Cell Biology, Fourth Military Medical University,Shaanxi,Xi'an,China,710032
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2023.02.015
  中图分类号：
- 纸质出版日期：2024，
  
  网络出版日期：2024-3-1，
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Ming-Yan Shi, Yarong Wang, Ying Shi, 等. SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer[J]. Genes & Diseases, 2024,11(2).

Ming-Yan Shi, Yarong Wang, Ying Shi, et al. SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer[J]. Genes & Diseases, 2024,11(2).
Ming-Yan Shi, Yarong Wang, Ying Shi, 等. SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer[J]. Genes & Diseases, 2024,11(2). DOI： 10.1016/j.gendis.2023.02.015.

Ming-Yan Shi, Yarong Wang, Ying Shi, et al. SETDB1-mediated CD147-K71 di-methylation promotes cell apoptosis in non-small cell lung cancer[J]. Genes & Diseases, 2024,11(2). DOI： 10.1016/j.gendis.2023.02.015.

摘要

Abstract

Protein post-translational modifications (PTMs) are at the heart status of cellular signaling events and broadly involved in tumor progression. CD147 is a tumor biomarker with various PTMs

promoting tumor metastasis and metabolism reprogramming. Nevertheless

the relationship between the PTMs of CD147 and apoptosis has not been reported. In our study

we produced a specific anti-CD147-K71 di-methylation (CD147-K71me2) antibody by immunizing with a di-methylated peptide and observed that the level of CD147-K71me2 in non-small cell lung cancer (NSCLC) tissues were lower than that in NSCLC adjacent tissues. SETDB1 was identified as the methyltransferase catalyzing CD147 to generate CD147-K71me2. RNA-seq showed that FOSB was the most significant differentially expressed gene (DEG) between wild-type CD147 (CD147-WT) and K71-mutant CD147 (CD147-K71R) groups. Subsequently

we found that CD147-K71me2 promoted the expression of FOSB by enhancing the phosphorylation of p38

leading to tumor cell apoptosis.

In vivo

experiments showed that CD147-K71me2 significantly inhibited tumor progression by promoting cell apoptosis. Taken together

our findings indicate the inhibitory role of CD147-K71me2 in tumor progression from the perspective of post-translational modification

which is distinct from the pro-cancer function of CD147 itself

broadening our perspective on tumor-associated antigen CD147.

关键词

Keywords

CD147 di-methylationCell apoptosisFOSBNon-small cell lung cancerSETDB1

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