Dos Santos Paulo Rodolfo Moraes, da Silva Gomes Paulo Ricardo, Romão Poliana, Maluf Feres Camargo, Guimarães Vanessa Ribeiro, Candido Patrícia, Gonçalves Guilherme Lopes, de Camargo Juliana Alves, Dos Santos Gabriel Arantes, Silva Iran, Leite Katia Ramos Moreira, Nahas William, Reis Sabrina T, Pimenta Ruan, Viana Nayara Izabel
Laboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Faculdade de Medicina, Universidade Anhembi Morumbi, São Paulo, SP, Brazil.
Biochem Genet. 2025 Feb;63(1):817-831. doi: 10.1007/s10528-024-10714-8. Epub 2024 Mar 24.
Bladder carcinoma (BC) is the tenth most frequent malignancy worldwide, with high morbidity and mortality rates. Despite recent treatment advances, high-grade BC and muscle-invasive BC present with significant progression and recurrence rates, urging the need for alternative treatments. The microRNA-21 (miR-21) has superexpression in many malignancies and is associated with cellular invasion and progression. One of its mechanisms of action is the regulation of RECK, a tumor suppressor gene responsible for inhibiting metalloproteinases, including MMP9. In a high-grade urothelial cancer cell line, we aimed to assess if miR-21 downregulation would promote RECK expression and decrease MMP9 expression. We also evaluated cellular migration and proliferation potential by inhibition of this pathway. In a T24 cell line, we inhibited miR-21 expression by transfection of a specific microRNA inhibitor (anti-miR-21). There were also control and scramble groups, the last with a negative microRNA transfected. After the procedure, we performed a genetic expression analysis of miR-21, RECK, and MMP9 through qPCR. Migration, proliferation, and protein expression were evaluated via wound healing assay, colony formation assay, flow cytometry, and immunofluorescence.After anti-miR-21 transfection, miR-21 expression decreased with RECK upregulation and MMP9 downregulation. The immunofluorescence assay showed a significant increase in RECK protein expression (p < 0.0001) and a decrease in MMP9 protein expression (p = 0.0101). The anti-miR-21 transfection significantly reduced cellular migration in the wound healing assay (p < 0.0001). Furthermore, in the colony formation assay, the anti-miR-21 group demonstrated reduced cellular proliferation (p = 0.0008), also revealed in the cell cycle analysis by flow cytometry (p = 0.0038). Our results corroborate the hypothesis that miR-21 is associated with BC cellular migration and proliferation, revealing its potential as a new effective treatment for this pathology.
膀胱癌(BC)是全球第十大常见恶性肿瘤,发病率和死亡率都很高。尽管近年来治疗取得了进展,但高级别BC和肌层浸润性BC的进展和复发率仍然很高,因此迫切需要替代治疗方法。微小RNA-21(miR-21)在许多恶性肿瘤中过表达,与细胞侵袭和进展相关。其作用机制之一是调节RECK,一种负责抑制金属蛋白酶(包括MMP9)的肿瘤抑制基因。在一个高级别尿路上皮癌细胞系中,我们旨在评估miR-21下调是否会促进RECK表达并降低MMP9表达。我们还通过抑制该途径评估细胞迁移和增殖潜力。在T24细胞系中,我们通过转染特异性微小RNA抑制剂(抗miR-21)来抑制miR-21表达。同时设置了对照组和乱序组,后者转染阴性微小RNA。实验操作后,我们通过qPCR对miR-21、RECK和MMP9进行基因表达分析。通过伤口愈合试验、集落形成试验、流式细胞术和免疫荧光评估迁移、增殖和蛋白质表达。抗miR-21转染后,miR-21表达下降,RECK上调,MMP9下调。免疫荧光试验显示RECK蛋白表达显著增加(p < 0.0001),MMP9蛋白表达下降(p = 0.0101)。在伤口愈合试验中,抗miR-21转染显著降低了细胞迁移(p < 0.0001)。此外,在集落形成试验中,抗miR-21组显示细胞增殖减少(p = 0.0008),流式细胞术细胞周期分析也显示了这一点(p = 0.0038)。我们的结果证实了miR-21与BC细胞迁移和增殖相关的假设,揭示了其作为这种疾病新的有效治疗方法的潜力。