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Aquaporins01:25

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  11. Aqp5 Promotes Epithelial-mesenchymal Transition And Tumor Growth Through Activating The Wnt/β-catenin Pathway In Triple-negative Breast Cancer

AQP5 promotes epithelial-mesenchymal transition and tumor growth through activating the Wnt/β-catenin pathway in triple-negative breast cancer

Zhengcai Zhu1, Tao Li1, Honggang Wang1

  • 1Department of General Surgery, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou, Jiangsu 215300, PR China.

Mutation Research
|July 3, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Aquaporin 5 (AQP5) promotes triple-negative breast cancer (TNBC) progression by enhancing cell proliferation, migration, and invasion via the Wnt/β-catenin pathway. Targeting AQP5 may offer a therapeutic strategy for TNBC.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Aquaporin 5 (AQP5) is implicated in various cancers, with overexpression linked to metastasis and poor prognosis.
  • Previous studies indicate high AQP5 expression in triple-negative breast cancer (TNBC) correlates with advanced stages.

Purpose of the Study:

  • To investigate the role of Aquaporin 5 (AQP5) in the oncogenesis and development of triple-negative breast cancer (TNBC).
  • To elucidate the molecular mechanisms by which AQP5 influences TNBC cell behavior.

Main Methods:

  • Established differential AQP5 expression systems in MDA-MB-231 cells using siRNA and overexpression vectors.
  • Assessed cell proliferation (CCK-8), apoptosis (FCM), migration (wound healing), and invasion (Transwell assays).
  • Analyzed epithelial-to-mesenchymal transition (EMT) markers via qRT-PCR and Western blot, and investigated the Wnt/β-catenin pathway using the inhibitor ICG-001.
Keywords:
Aquaporin 5Triple-negative breast cancerWnt/β-catenin pathway

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Main Results:

  • AQP5 overexpression significantly promoted TNBC cell proliferation, migration, and invasion while inhibiting apoptosis.
  • AQP5 up-regulation increased Bcl-2 and decreased Caspase-3 expression, indicating altered apoptosis regulation.
  • Overexpressed AQP5 induced EMT-related factors and activated the Wnt/β-catenin pathway, evidenced by increased nuclear β-catenin and reversed by ICG-001.

Conclusions:

  • AQP5 enhances TNBC cell proliferation, migration, and invasion by modulating EMT-related proteins via Wnt/β-catenin pathway activation.
  • AQP5 plays a critical role in TNBC progression, suggesting it as a potential therapeutic target.