Adipose mesenchymal stem cell conditioned medium and extract: A promising therapeutic option for regenerative breast cancer therapy.

INTRODUCTION

Breast cancer is the second most common cancer and a leading cause of cancer death in U.S. women. The tumor microenvironment, especially nearby adipocytes, plays a crucial role in its progression. Therefore, this study aimed to investigate the effects of human adipose mesenchymal stem cells-derived conditioned medium (SUP) and extract (CE) from on breast cancer cells.

METHODS

Human adipose-derived mesenchymal stem cells were isolated and characterized by flow cytometry using Cluster of Differentiation (CD) markers (CD34, CD45, CD90, and CD105). The differentiation potential was confirmed via adipogenic and osteogenic induction. MCF-7 and MDA-MB-231 cells were treated with SUP and CE, and cell viability was assessed using the 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay at 24, 48, and 72 h. Doubling time, colony formation, wound healing, and gene expression for key cancer-related genes (, , , , , , caspase 3, and caspase 9) were also evaluated.

RESULTS

Both SUP and CE significantly inhibited the viability of MCF-7 and MDA-MB-231 cells, reduced their doubling time, and suppressed colony formation. In wound healing assays, cell migration was notably impaired in MDA-MB-231 cells but less so in MCF-7 cells. Real-time polymerase chain reaction revealed downregulation of TIMP1, MMP2, PDL1, and IDO in MDA-MB-231 cells after treatment, while CE increased certain gene expressions in MCF-7 cells. Bax, caspase 3, and caspase 9 expressions were significantly upregulated in MDA-MB-231 cells but not in MCF-7 cells after treatment.

CONCLUSION

Human adipose-derived mesenchymal stem cells-derived SUP and CE exhibit antitumor effects on breast cancer cells, suggesting a potential therapeutic strategy to suppress tumor progression. Mesenchymal stem cells-SUP and CE could be a safe and novel regenerative approach for breast reconstruction postmastectomy without tumor recurrence risk.