It is becoming increasingly evident that mesenchymal stem/stromal cells are recruited by cancer cells from nearby endogenous host stroma and promote events such as tumor proliferation, angiogenesis, invasion, and metastasis, as well as mediate therapeutic resistance. Consequently, understanding the regulatory mechanisms of ASCs that influence the tumor microenvironment may provide an avenue for further treatment. To understand the role of the ASC secretome in breast cancer cell proliferation, death, and phenotype alteration, adipose-derived stem cell-conditioned medium (mASC) was used to cultivate MCF-7 and MDA-MB-231 cells. These breast cancer cells in mASC showed a shorter doubling time, higher frequency of EdU positivity, and higher levels of phosphorylated histone 3. In addition, increased expression of cyclin B1 was observed, suggesting that proliferation was induced. The mASC was also able to increase apoptosis in MCF-7 cells, which was confirmed by caspase-7 activation. The number of tumor-initiating cells (CD44⁺ CD24^-/low) and migration capacity were increased in cells cultivated in mASC. These data collectively suggest that ASC-conditioned medium can induce selective pressure by increasing cell proliferation, giving rise to a more aggressive phenotype in MCF-7 and MDA-MB-231 cells. Our study provides a foundation for further elucidation of the precise mechanism underlying ASCs in breast cancer cells and the modulation of ASCs in potential therapeutic uses.

越来越明显的是，间充质干/基质细胞被癌细胞从附近的内源性宿主基质中募集，并促进肿瘤增殖、血管生成、侵袭和转移等事件，以及介导治疗耐药性。因此，了解影响肿瘤微环境的 ASC 的调节机制可能为进一步治疗提供途径。为了了解 ASC 分泌组在乳腺癌细胞增殖、死亡和表型改变中的作用，使用脂肪干细胞条件培养基 (mASC) 培养 MCF-7 和 MDA-MB-231 细胞。mASC 中的这些乳腺癌细胞显示出更短的倍增时间、更高的 EdU 阳性频率和更高水平的磷酸化组蛋白 3。此外，还观察到细胞周期蛋白 B1 的表达增加，表明诱导增殖。mASC 还能够增加 MCF-7 细胞的凋亡，这通过 caspase-7 激活得到证实。肿瘤起始细胞（CD44⁺ CD24 ^-/low ) 和迁移能力在 mASC 中培养的细胞中增加。这些数据共同表明 ASC 条件培养基可以通过增加细胞增殖来诱导选择压力，从而在 MCF-7 和 MDA-MB-231 细胞中产生更具攻击性的表型。我们的研究为进一步阐明乳腺癌细胞中 ASC 的确切机制以及 ASC 在潜在治疗用途中的调节提供了基础。