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TRAIL suppresses human breast cancer cell migration via MADD/CXCR7

Rui Wang1, Jin-Cheng Li

  • 1Department of Breast and Thyroid Sugery, The First Affiliated Hospital of Liaoning Medical University. Jinzhou, Liaoning, China E-mail : wangr0428@163.com, lijcwr@163.com.

Asian Pacific Journal of Cancer Prevention : APJCP
|April 10, 2015
PubMed
Abstract

Insights

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) influences breast cancer cell migration. MADD and CXCR7 regulate this process, with MADD acting upstream of CXCR7 in a novel signaling pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) shows promise in cancer therapy by inducing apoptosis in cancer cells.
  • TRAIL also influences non-apoptotic signals, including metastasis, autophagy, and proliferation, but its mechanisms remain unclear.
  • Understanding TRAIL's non-apoptotic effects is crucial for developing effective cancer treatments.

Purpose of the Study:

  • To investigate the roles of MADD and CXCR7 in TRAIL-mediated breast cancer cell migration.
  • To elucidate the signaling pathway involving MADD/CXCR7 in breast cancer metastasis.

Main Methods:

  • Transwell migration assays were used to evaluate cell migration.
  • Quantitative RT-PCR and Western blotting assessed gene and protein expression.
  • Knockdown and overexpression experiments determined the regulatory functions of MADD and CXCR7.

Main Results:

  • TRAIL treatment increased MADD and CXCR7 expression in breast cancer cells.
  • Knockdown of MADD enhanced TRAIL-induced cell migration, while CXCR7 positively regulated TRAIL-inhibited migration.
  • MADD was identified as an upstream regulator of TRAIL-induced CXCR7 expression, revealing a negative feedback loop between MADD and CXCR7.

Conclusions:

  • A novel signaling pathway involving MADD and CXCR7 in the regulation of breast cancer cell migration was defined.
  • This pathway provides new insights into the mechanisms of cancer metastasis.
  • Targeting this pathway could offer therapeutic strategies for breast cancer treatment.

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