2. Academic Validation
  3. Cryptochrome 2 acetylation attenuates its antiproliferative effect in breast cancer

Cryptochrome 2 acetylation attenuates its antiproliferative effect in breast cancer

  • Cell Death Dis. 2023 Apr 6;14(4):250. doi: 10.1038/s41419-023-05762-8.
Kangkai Xia # 1,  Shujing Li # 1,  Yuxi Yang 1,  Xiaoxia Shi 1,  Binggong Zhao 1,  Linlin Lv 1,  Zhiqiang Xin 2,  Jie Kang 1,  Ping Ren 3,  Huijian Wu 4
Affiliations

Affiliations

  • 1 School of Bioengineering & Key Laboratory of Protein Modification and Disease, Liaoning Province, Dalian University of Technology, Dalian, 116024, China.
  • 2 The Second Hospital of Dalian Medical University, Dalian, 116024, China.
  • 3 The Second Hospital of Dalian Medical University, Dalian, 116024, China. dlrenping@dmu.edu.cn.
  • 4 School of Bioengineering & Key Laboratory of Protein Modification and Disease, Liaoning Province, Dalian University of Technology, Dalian, 116024, China. wuhj@dlut.edu.cn.
  • # Contributed equally.
PMID: 37024472 DOI: 10.1038/s41419-023-05762-8
Abstract

Breast Cancer is the most commonly diagnosed Cancer, and its global impact is increasing. Its onset and progression are influenced by multiple cues, one of which is the disruption of the internal circadian clock. Cryptochrome 2 (Cry2) genetic dysregulation may lead to the development of some diseases and even tumors. In addition, post-translational modifications can alter the Cry2 function. Here, we aimed to elucidate the post-translational regulations of Cry2 and its role in breast Cancer pathogenesis. We identified p300-drived acetylation as a novel Cry2 post-translational modification, which histone deacetylase 6 (HDAC6) could reverse. Furthermore, we found that Cry2 inhibits breast Cancer proliferation, but its acetylation impairs this effect. Finally, bioinformatics analysis revealed that genes repressed by Cry2 in breast Cancer were mainly enriched in the NF-κB pathway, and acetylation reversed this repression. Collectively, these results indicate a novel Cry2 regulation mechanism and provide a rationale for its role in breast tumorigenesis.

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