Adipsin-dependent adipocyte maturation induces cancer cell invasion in breast cancer.
Jumpei YoshidaTakanori HayashiEiji MunetsunaBehnoush KhaledianFujiko SueishiMasahiro MizunoMasao MaedaTakashi WatanabeKaori UshidaEiji SugiharaKazuyoshi ImaizumiKenji KawadaNaoya AsaiYohei ShimonoPublished in: Scientific reports (2024)
Adipocyte-cancer cell interactions promote tumor development and progression. Previously, we identified adipsin (CFD) and its downstream effector, hepatocyte growth factor (HGF), as adipokines that enhance adipocyte-breast cancer stem cell interactions. Here, we show that adipsin-dependent adipocyte maturation and the subsequent upregulation of HGF promote tumor invasion in breast cancers. Mature adipocytes, but not their precursors, significantly induced breast tumor cell migration and invasion in an adipsin expression-dependent manner. Promoters of tumor invasion, galectin 7 and matrix metalloproteinases, were significantly upregulated in cancer cells cocultured with mature adipocytes; meanwhile, their expression levels in cancer cells cocultured with adipocytes were reduced by adipsin knockout (Cfd KO) or a competitive inhibitor of CFD. Tumor growth and distant metastasis of mammary cancer cells were significantly suppressed when syngeneic mammary cancer cells were transplanted into Cfd KO mice. Histological analyses revealed reductions in capsular formation and tumor invasion at the cancer-adipocyte interface in the mammary tumors formed in Cfd KO mice. These findings indicate that adipsin-dependent adipocyte maturation may play an important role in adipocyte-cancer cell interaction and breast cancer progression.
Keyphrases
- adipose tissue
- insulin resistance
- fatty acid
- high fat diet induced
- growth factor
- poor prognosis
- papillary thyroid
- type diabetes
- single cell
- stem cells
- squamous cell carcinoma
- cancer stem cells
- signaling pathway
- dendritic cells
- childhood cancer
- bone marrow
- endothelial cells
- squamous cell
- cell therapy
- lymph node metastasis
- young adults
- long non coding rna
- oxidative stress
- mesenchymal stem cells
- diabetic rats