2. Academic Validation
  3. AURKAIP1 actuates tumor progression through stabilizing DDX5 in triple negative breast cancer

AURKAIP1 actuates tumor progression through stabilizing DDX5 in triple negative breast cancer

  • Cell Death Dis. 2023 Dec 1;14(12):790. doi: 10.1038/s41419-023-06115-1.
Wenwen Tian # 1 2,  Yuhui Tang # 1,  Yongzhou Luo # 1,  Jindong Xie 1,  Shaoquan Zheng 3,  Yutian Zou 1,  Xiaojia Huang 2,  Linyu Wu 1,  Junsheng Zhang 1,  Yuying Sun 1,  Hailin Tang 1,  Wei Du 4,  Xing Li 5,  Xiaoming Xie 6
Affiliations

Affiliations

  • 1 Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, 651 East Dongfeng Road, Guangzhou, 510060, China.
  • 2 Affiliated Cancer Hosipital & Institute of Guangzhou Medical University, No.78 Hengzhigang Road, Guangzhou, 510095, China.
  • 3 Breast Disease Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
  • 4 Department of pathology, The First People's Hospital of Changde City, Changde, Hunan, China. dw417@sina.com.
  • 5 Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, 651 East Dongfeng Road, Guangzhou, 510060, China. lixing@sysucc.org.cn.
  • 6 Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, 651 East Dongfeng Road, Guangzhou, 510060, China. xiexm@sysucc.org.cn.
  • # Contributed equally.
PMID: 38040691 DOI: 10.1038/s41419-023-06115-1
Abstract

Aurora-A kinase interacting protein 1 (AURKAIP1) has been proved to take an intermediary role in Cancer by functioning as a negative regulator of Aurora-A kinase. However, it remains unclear whether and how AURKAIP1 itself would directly engage in regulating malignancies. The expression levels of AURKAIP1 were detected in triple negative breast Cancer (TNBC) by immunohistochemistry and western blots. The CCK8, colony formation assays and nude mouse model were conducted to determine cell proliferation whereas transwell and wound healing assays were performed to observe cell migration. The interaction of AURKAIP1 and DEAD-box helicase 5 (DDX5) were verified through co-immunoprecipitation and successively western blots. From the results, we found that AURKAIP1 was explicitly upregulated in TNBC, which was positively associated with tumor size, lymph node metastases, pathological stage and unfavorable prognosis. AURKAIP1 silencing markedly inhibited TNBC cell proliferation and migration in vitro and in vivo. AURKAIP1 directly interacted with and stabilized DDX5 protein by preventing ubiquitination and degradation, and DDX5 overexpression successfully reversed proliferation inhibition induced by knockdown of AURKAIP1. Consequently, AURKAIP1 silencing suppressed the activity of Wnt/β-catenin signaling in a DDX5-dependent manner. Our study may primarily disclose the molecular mechanism by which AURKAIP1/DDX5/β-catenin axis modulated TNBC progression, indicating that AURKAIP1 might serve as a therapeutic target as well as a TNBC-specific biomarker for prognosis.

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