Nguyen Huonggiang, Huang Qingzhi, Juang Uijin, Gwon Suhwan, Jung Woohyeong, Lee Soohyeon, Lee Beomwoo, Kwon So Hee, Kim In Soo, Park Jongsun, Kim Seon-Hwan
Department of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Department of Medical Science, Metabolic Syndrome and Cell Signaling Laboratory, Institute for Cancer Research, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Front Oncol. 2024 Oct 8;14:1435605. doi: 10.3389/fonc.2024.1435605. eCollection 2024.
The mutated in colorectal cancer (MCC) gene was initially identified as a candidate tumor suppressor gene in colorectal cancer, acting as a negative regulator of cell cycle progression. However, its functional roles in brain tumors, particularly glioblastoma, remain largely unexplored. This study reveals a significant association between MCC status and glioblastoma.
We explored MCC expression in the glioblastoma database, patient samples, and cell lines. We investigated the proliferation and migration of the cell lines in MCC gene knockdown using small interfering RNA.
analyses revealed elevated protein and mRNA levels of MCC in several glioblastoma cell lines (U118MG and T98G). Silencing MCC expression via siRNA-mediated knockdown resulted in increased proliferation and migration of these cell lines. Supporting these findings, analyses of The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), and Genotype-Tissue Expression (GTEx) databases confirmed higher MCC expression in glioblastoma tumors than in normal brain tissue. Importantly, we observed that high MCC expression was associated with poor prognosis in glioblastoma patients, highlighting its potential role in disease progression. Additionally, this study identifies a nuclear localization of MCC in the glioblastoma cell line.
These findings indicate that MCC expression is significantly upregulated in glioblastoma and may play a role in its pathophysiology, warranting further investigation.
结直肠癌突变基因（MCC）最初被鉴定为结直肠癌中的候选肿瘤抑制基因，作为细胞周期进程的负调节因子。然而，其在脑肿瘤，特别是胶质母细胞瘤中的功能作用仍 largely 未被探索。本研究揭示了MCC状态与胶质母细胞瘤之间的显著关联。
我们在胶质母细胞瘤数据库、患者样本和细胞系中探索了MCC表达。我们使用小干扰RNA研究了MCC基因敲低时细胞系的增殖和迁移。
分析显示在几种胶质母细胞瘤细胞系（U118MG和T98G）中MCC的蛋白质和mRNA水平升高。通过siRNA介导的敲低使MCC表达沉默导致这些细胞系的增殖和迁移增加。支持这些发现的是，对癌症基因组图谱（TCGA）、中国胶质瘤基因组图谱（CGGA）和基因型-组织表达（GTEx）数据库的分析证实胶质母细胞瘤肿瘤中MCC表达高于正常脑组织。重要的是，我们观察到胶质母细胞瘤患者中高MCC表达与不良预后相关，突出了其在疾病进展中的潜在作用。此外，本研究确定了MCC在胶质母细胞瘤细胞系中的核定位。
这些发现表明MCC表达在胶质母细胞瘤中显著上调，可能在其病理生理学中起作用，值得进一步研究。
