GPD2: The relationship with cancer and neural stemness

IF 3.9 4区生物学 Q4 Biochemistry, Genetics and Molecular Biology Cells and Development Pub Date : 2023-03-01 DOI:10.1016/j.cdev.2022.203824

Maimaiti Mikeli , Makoto Fujikawa , Tsutomu Tanabe

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Abstract

We previously reported that knocking down GPD2 (glycerol-3-phosphate dehydrogenase 2), responsible for the glycerol-phosphate shuttle, causes human hepatocarcinoma-derived HuH-7 cells, lowering the cancer stemness. After examining whether GPD2 expression in the other cell lines could affect their cancer stemness, this study showed that human neuroblastoma-derived SH-SY5Y cells also lower the ability of sphere formation by knocking down GPD2. This suggests that GPD2 relates to the common mechanism for maintaining cancer stem cells, as in the cases like SH-SY5Y and HuH-7 cells. In addition, knocking down GPD2 in SH-SY5Y cells showed a morphological change and increasing tendency of neuronal marker genes, including GAP43, NeuN, and TUBB3, indicating that GPD2 may contribute to not only cancer but also neural stem cell maintenance. After all, GPD2 may play a role in maintaining cancer and neural stemness, although further rigorous studies are essential to conclude this. It is expected that GPD2 will be a novel target gene for cancer therapy, stem cell research, and development.

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GPD2:与肿瘤和神经干性的关系

我们之前报道，敲低GPD2（甘油-3-磷酸脱氢酶2），负责甘油-磷酸穿梭，导致人类肝癌衍生的HuH-7细胞，降低癌症的干性。在检测了GPD2在其他细胞系中的表达是否会影响其癌症干性后，本研究表明，人类神经母细胞瘤衍生的SH-SY5Y细胞也通过敲低GPD2来降低球体形成的能力。这表明GPD2与维持癌症干细胞的常见机制有关，如SH-SY5Y和HuH-7细胞。此外，在SH-SY5Y细胞中敲除GPD2显示了包括GAP43、NeuN和TUBB3在内的神经元标记基因的形态学变化和增加趋势，表明GPD2不仅有助于癌症，而且有助于神经干细胞的维持。毕竟，GPD2可能在维持癌症和神经干度方面发挥作用，尽管需要进一步的严格研究才能得出结论。GPD2有望成为癌症治疗、干细胞研究和开发的新靶基因。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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