Department of Integrative Medical Biology, Section of Anatomy, Umeå University, Umeå, Sweden.
Department of Integrative Medical Biology, Section of Anatomy, Umeå University, Umeå, Sweden; Department of Surgical & Perioperative Sciences, Plastic Surgery and Surgery, Umeå University, Umeå, Sweden.
J Plast Reconstr Aesthet Surg. 2023 Aug;83:69-76. doi: 10.1016/j.bjps.2023.05.006. Epub 2023 May 7.
Although autologous fat grafting is considered a successful method for the management of contour deformities, the fat graft could potentially induce cancer reappearance by fueling dormant breast cancer cells. Our aim was to characterize the role of adipose-derived stem cells on active and dormant breast cancer cell growth.
Cobalt chloride was used to induce dormancy in MCF-7 cancer cells. Proliferation of active and dormant cancer cells was determined in the presence of adipose-derived stem cells. A proteome array was used to detect cancer-related protein expression in the cell-conditioned medium. The migration of cancer cells was measured in response to conditioned medium from the adipose-derived stem cells.
The adipose-derived stem cells showed variable effects on active MCF-7 cells growth and inhibited MCF-7 proliferation after the withdrawal of cobalt chloride. Of the 84 different proteins measured in the conditioned medium, only tenascin-C was differentially expressed in the co-cultures. MCF-7 cells alone did not express tenascin-C, whereas co-cultures between MCF-7 and adipose-derived stem cells expressed more tenascin-C versus adipose-derived stem cells alone. The conditioned medium from co-cultures significantly increased the migration of the cancer cells.
Adipose-derived stem cells themselves neither increased the growth or migration of cancer cells, suggesting that autologous fat grafting may be oncologically safe if reconstruction is postponed until there is no evidence of active disease. However, interactions between adipose-derived stem cells and MCF-7 cancer cells could potentially lead to the production of factors, which further promote cancer cell migration.
尽管自体脂肪移植被认为是一种成功的方法来管理轮廓畸形，但脂肪移植可能通过为休眠的乳腺癌细胞提供营养而导致癌症复发。我们的目的是研究脂肪来源干细胞对活跃和休眠乳腺癌细胞生长的作用。
使用钴氯化物诱导 MCF-7 癌细胞休眠。在脂肪来源干细胞存在的情况下，测定活跃和休眠癌细胞的增殖。使用蛋白质组芯片检测细胞条件培养基中与癌症相关的蛋白表达。测量癌细胞对脂肪来源干细胞条件培养基的迁移反应。
脂肪来源干细胞对活跃的 MCF-7 细胞生长有不同的影响，并在钴氯化物去除后抑制 MCF-7 增殖。在测量的 84 种不同蛋白质中，只有 tenascin-C 在共培养物中差异表达。单独的 MCF-7 细胞不表达 tenascin-C，而 MCF-7 和脂肪来源干细胞之间的共培养物表达的 tenascin-C 多于单独的脂肪来源干细胞。共培养物的条件培养基显著增加了癌细胞的迁移。
脂肪来源干细胞本身既不会增加癌细胞的生长或迁移，这表明如果重建推迟到没有活跃疾病的证据，那么自体脂肪移植在肿瘤学上可能是安全的。然而，脂肪来源干细胞和 MCF-7 癌细胞之间的相互作用可能会导致产生进一步促进癌细胞迁移的因子。
