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

Area of Science:

• Oncology
• Molecular Biology
• Cancer Research

Background:

• Aurora-A kinase interacting protein 1 (AURKAIP1) regulates Aurora-A kinase activity in cancer.
• The direct role of AURKAIP1 in cancer malignancy remains largely uncharacterized.

Purpose of the Study:

• To investigate the role and molecular mechanism of AURKAIP1 in triple-negative breast cancer (TNBC) progression.
• To explore AURKAIP1 as a potential therapeutic target and prognostic biomarker in TNBC.

Main Methods:

• Immunohistochemistry and western blots to assess AURKAIP1 expression in TNBC tissues.
• In vitro (CCK8, colony formation, transwell, wound healing) and in vivo (nude mouse model) assays to evaluate proliferation and migration.
• Co-immunoprecipitation and western blots to confirm the interaction between AURKAIP1 and DEAD-box helicase 5 (DDX5).

Main Results:

• AURKAIP1 expression is significantly upregulated in TNBC and correlates with tumor size, lymph node metastasis, pathological stage, and poor prognosis.
• AURKAIP1 silencing inhibits TNBC cell proliferation and migration both in vitro and in vivo.
• AURKAIP1 interacts with and stabilizes DDX5 by inhibiting its ubiquitination and degradation.
• DDX5 overexpression rescues the inhibitory effects of AURKAIP1 knockdown on proliferation.
• AURKAIP1 silencing suppresses Wnt/β-catenin signaling activity in a DDX5-dependent manner.

Conclusions:

• AURKAIP1 plays a crucial role in promoting TNBC progression through the AURKAIP1/DDX5/β-catenin signaling axis.
• AURKAIP1 functions as an oncogene in TNBC, highlighting its potential as a therapeutic target.
• AURKAIP1 serves as a promising TNBC-specific biomarker for predicting patient prognosis.