Feng Cheng'ao, Fan Yu, Gao Hongwei, Zhang Bowen, Lu Xiaojie
Wuxi School of Medicine, Neuroscience Center, Jiangnan University, Wuxi, Jiangsu, PR China.
Department of Neurosurgery, Jiangnan University Medical Center, Wuxi, Jiangsu, PR China.
Biomark Med. 2025 Mar;19(6):205-213. doi: 10.1080/17520363.2025.2473131. Epub 2025 Mar 4.
This study mainly explored the regulatory role and mechanism of MCCC2 in GBM.
This study verified the expression in clinical samples and GBM cell lines. CCK-8 and cell cloning experiments, flow cytometry, scratch experiments and Transwell chamber experiments were used to detect the effects of MCCC2 expression on proliferation, apoptosis, migration and invasion of GBM cells.
A reduction in MCCC2 expression could significantly lower the protein levels of ERK, decrease p-ERK levels, and inhibit ERK phosphorylation. Ulixertinib, an ERK inhibitor, was shown to hinder the proliferation, migration, and invasion of GBM cells and counteract the regulatory impact of MCCC2 overexpression on GBM cells.
This investigation revealed that suppressing MCCC2 expression impedes the proliferation, migration, and invasion of GBM cells and promotes GBM cell apoptosis by curtailing ERK expression and phosphorylation. This discovery implies that MCCC2 might serve as a potential biological target for anti-GBM therapy, laying the groundwork for future research in this field.
本研究主要探讨MCCC2在胶质母细胞瘤（GBM）中的调控作用及机制。
本研究验证了其在临床样本和GBM细胞系中的表达。采用CCK-8和细胞克隆实验、流式细胞术、划痕实验和Transwell小室实验检测MCCC2表达对GBM细胞增殖、凋亡、迁移和侵袭的影响。
MCCC2表达降低可显著降低ERK蛋白水平，降低p-ERK水平，并抑制ERK磷酸化。ERK抑制剂Ulixertinib被证明可阻碍GBM细胞的增殖、迁移和侵袭，并抵消MCCC2过表达对GBM细胞的调控作用。
本研究表明，抑制MCCC2表达可通过减少ERK表达和磷酸化来阻碍GBM细胞的增殖、迁移和侵袭，并促进GBM细胞凋亡。这一发现意味着MCCC2可能成为抗GBM治疗的潜在生物学靶点，为该领域的未来研究奠定了基础。
