Frontiers in Oncology (Oct 2024)

The mutated in colorectal cancer (MCC) gene can serve as a potential biomarker of glioblastoma

  • Huonggiang Nguyen,
  • Huonggiang Nguyen,
  • Qingzhi Huang,
  • Qingzhi Huang,
  • Uijin Juang,
  • Uijin Juang,
  • Suhwan Gwon,
  • Suhwan Gwon,
  • Woohyeong Jung,
  • Woohyeong Jung,
  • Soohyeon Lee,
  • Soohyeon Lee,
  • Beomwoo Lee,
  • Beomwoo Lee,
  • So Hee Kwon,
  • In Soo Kim,
  • In Soo Kim,
  • Jongsun Park,
  • Jongsun Park,
  • Seon-Hwan Kim

DOI
https://doi.org/10.3389/fonc.2024.1435605
Journal volume & issue
Vol. 14

Abstract

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IntroductionThe 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.MethodsWe 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.ResultsIn vitro 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.DiscussionThese findings indicate that MCC expression is significantly upregulated in glioblastoma and may play a role in its pathophysiology, warranting further investigation.

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