Computational Biology and Systems Biomedicine Group, Biodonostia Health Research Institute, Calle Doctor 8 Beguiristain s/n, 20014 San Sebastián, Spain; Computational Biomedicine Data Analysis Platform, Biodonostia Health Research Institute, C/ Doctor 8 Beguiristain s/n, 20014 San Sebastián, Spain.
Department of Cell Biology and Histology, Faculty of Medicine and Nursing, University of the Basque Country, 48940 Leioa, Spain; Univ. Bordeaux, INSERM, LAMC, U1029, F-33600 Pessac, France.
Biochim Biophys Acta Mol Cell Res. 2021 Mar;1868(3):118912. doi: 10.1016/j.bbamcr.2020.118912. Epub 2020 Nov 26.
Despite continuous exertion made, colon cancer still represents a major health problem and its incidence continues being high worldwide. There is growing evidence in support of the cancer stem cells (CSCs) being central in the initiation of this cancer, and CSCs have been the focus of various studies for the identification of new ways of treatment. Lately, the proprotein convertases (PCs) were reported to regulate the maturation and expression of various molecules involved in the malignant phenotype of colon cancer cells, however, the identity of the molecules regulated by these serine proteases in CSCs is unknown. In this study, we used the general PCs inhibitor, the Decanoyl-RVKR-chloromethylketone (Decanoyl-RVKR-CMK) that inhibits all the PCs found in the secretory pathway, and analyzed its effect on CSCs using RNA-seq analysis. Remarkably, from the only 9 up-regulated genes in the human SW620-derived sphere-forming cells, we identified 7 of the 11 human metallothioneins, all of them localized on chromosome 16, and zinc related proteins as downstream effectors of the PCs. The importance of these molecules in the regulation of cell proliferation, differentiation and chemoresistance, and their reported potential tumor suppressor role and loss in colon cancer patients associated with worse prognosis, suggests that targeting PCs in the control of the malignant phenotype of CSCs is a new potential therapeutic strategy in colon cancer.
尽管不断努力,结肠癌仍然是一个主要的健康问题,其发病率在全球范围内仍然很高。越来越多的证据支持癌症干细胞(CSCs)在癌症的发生中起核心作用,CSCs 一直是各种研究的焦点,以寻找新的治疗方法。最近,报道蛋白水解酶(PCs)调节参与结肠癌细胞恶性表型的各种分子的成熟和表达,然而,这些丝氨酸蛋白酶在 CSCs 中调节的分子的身份尚不清楚。在这项研究中,我们使用了通用 PCs 抑制剂,十一烷酰基-RVKR-氯甲基酮(Decanoyl-RVKR-CMK),它抑制了分泌途径中发现的所有 PCs,并通过 RNA-seq 分析来分析其对 CSCs 的影响。值得注意的是,在人源性 SW620 球体形成细胞中仅上调的 9 个基因中,我们鉴定出 11 个人类金属硫蛋白中的 7 个,它们都定位于 16 号染色体上,以及锌相关蛋白作为 PCs 的下游效应物。这些分子在细胞增殖、分化和化疗耐药性中的重要作用,以及它们在结肠癌患者中报道的潜在肿瘤抑制作用和丢失与预后不良相关,表明在控制 CSCs 的恶性表型方面靶向 PCs 是结肠癌的一种新的潜在治疗策略。