Department of Clinical and Experimental Biomedical Sciences "Mario Serio", Section of Experimental Pathology and Oncology, University of Florence, Florence, Italy.
Department of NEUROFARBA, University of Florence, Florence, Italy.
J Enzyme Inhib Med Chem. 2020 Dec;35(1):1185-1193. doi: 10.1080/14756366.2020.1764549.
Mesenchymal stem cells (MSC) take part to solid tumour-associated stroma and critically influence progression of malignancy. Our study represents a striking example of melanoma progression to a more malignant and resistant phenotype promoted by MSC and the possibility to contrast this diabolic liaison using CAIX inhibitors. In particular, we demonstrated that melanoma cells exposed to a MSC-conditioned medium switch to a more malignant phenotype, characterised by resistance to programmed cell death and endowed with an epithelial-to-mesenchymal transition and stem cell characteristics. These effects were reversed abrogating MSC CAIX activity using SLC-0111, a CAIX inhibitor. Moreover, the acquisition by melanoma cells of a Vemurafenib-resistant phenotype upon MSC-conditioned medium exposure was removed when MSC were treated with SLC-0111. Therefore, MSC may profoundly reprogramme melanoma cells towards a wide resistant phenotype through CAIX involvement, as the use of SLC-0111 is able to contrast the development of this highly risky adaptation for disease progression.
间充质干细胞 (MSC) 参与实体瘤相关基质,并对恶性肿瘤的进展起关键作用。我们的研究代表了一个显著的例子,即 MSC 促进黑色素瘤向更恶性和更具耐药性的表型进展,以及使用 CAIX 抑制剂来对抗这种恶性循环的可能性。具体而言,我们证明了暴露于 MSC 条件培养基中的黑色素瘤细胞会转变为更恶性的表型,其特征是对程序性细胞死亡的抵抗,并具有上皮间质转化和干细胞特征。使用 CAIX 抑制剂 SLC-0111 阻断 MSC 的 CAIX 活性可以逆转这些作用。此外,当用 SLC-0111 处理 MSC 时,暴露于 MSC 条件培养基的黑色素瘤细胞获得的威罗非尼耐药表型也被消除。因此,MSC 可能通过 CAIX 的参与,将黑色素瘤细胞深刻地重新编程为广泛的耐药表型,因为 SLC-0111 的使用能够对抗这种对疾病进展具有高度风险的适应性发展。