Lipolysis-stimulated lipoprotein receptor is involved in fatty acid binding protein 4-mediated prostate cancer cell growth in bone
- 1Department of Anatomy and Cell Biology, Faculty of Pharmacy, Research Institute of Pharmaceutical Sciences, Musashino University, Tokyo, Japan.
- 2Department of Oral Molecular Pathology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
- 3Division of Pathology, Tokushima University Hospital, Tokushima, Japan.
- 0Department of Anatomy and Cell Biology, Faculty of Pharmacy, Research Institute of Pharmaceutical Sciences, Musashino University, Tokyo, Japan.
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View abstract on PubMed
Summary
This summary is machine-generated.Fatty acid binding protein 4 (FABP4) promotes prostate cancer progression. Its binding with lipolysis-stimulated lipoprotein receptor (LSR) activates Akt signaling, impacting tumor growth in the bone microenvironment.
Area Of Science
- Oncology
- Molecular Biology
- Endocrinology
Background
- Obesity-associated adipokines, like FABP4, are linked to prostate cancer malignancy and mortality.
- Previous research established FABP4's role in promoting prostate cancer cell growth and invasion.
Purpose Of The Study
- To identify novel binding partners of FABP4 involved in prostate cancer progression.
- To elucidate the molecular mechanisms by which FABP4 influences prostate cancer in the bone microenvironment.
Main Methods
- Investigated the interaction between FABP4 and lipolysis-stimulated lipoprotein receptor (LSR) using prostate cancer cell models.
- Utilized knockdown techniques (LSR KD) to assess the role of LSR in Akt phosphorylation.
- Performed intraosseous injections of modified cancer cells in vivo to evaluate tumor growth and markers.
- Co-cultured prostate cancer cells with bone marrow stromal cells (BMSCs) to study FABP4 secretion.
Main Results
- Lipolysis-stimulated lipoprotein receptor (LSR) was identified as a novel binding partner for FABP4.
- FABP4-LSR binding induced Akt phosphorylation; LSR knockdown prevented this activation.
- LSR knockdown prostate cancer cells exhibited reduced intraosseous tumor size, proliferation (Ki-67), and phospho-Akt levels.
- Bone marrow stromal cells (BMSCs) secreted FABP4 upon co-culture with prostate cancer cells.
Conclusions
- FABP4-LSR binding is a critical signaling pathway regulating prostate cancer cell progression.
- The FABP4-LSR interaction mediates prostate cancer cell signaling within the bone microenvironment.
- Targeting the FABP4-LSR interaction may offer therapeutic strategies for prostate cancer.
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