Background

Oral cancer is a very familiar tumor together with a gravely effect on the life of human. GPD1 has been verified to join into the regulation of multifold cancers’ progression through being a suppressor. Interestingly, it has been revealed that GPD1 overexpression activated the PI3K/AKT signaling pathway. However, the regulatory functions of GPD1 on the PI3K/AKT/GSK-3β pathway in oral cancer progression keep vague, and need more investigations.

Objectives

To investigate the regulation function and mechanism of GPD1 in oral cancer.

Results

It was demonstrated that GPD1 exhibited lower expression in oral cancer. Moreover, overexpression of GPD1 relieved cell proliferation and strengthened cell apoptosis in oral cancer. Overexpression of GPD1 weakened cell migration and invasion in oral cancer. In addition, it was confirmed that overexpression of GPD1 suppressed mitochondrial function in oral cancer. At last, it was illustrated that GPD1 triggered the PI3K/AKT/GSK-3β pathway.

Conclusion

For the first time, this work manifested that GPD1 inhibited the proliferation, migration and invasion of oral cancer cells by inhibiting mitochondrial function through triggering the PI3K/AKT/GSK-3β pathway. This discovery hinted that GPD1 may be a serviceable biomarker for the treatment of oral cancer.

中文翻译：

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GPD1通过抑制线粒体功能减轻口腔癌细胞的增殖、迁移和侵袭能力

背景

口腔癌是一种常见的肿瘤，严重影响人类的生活。 GPD1 已被证实可以通过抑制作用参与多种癌症进展的调节。有趣的是，研究表明 GPD1 过度表达会激活 PI3K/AKT 信号通路。然而，GPD1在口腔癌进展中对PI3K/AKT/GSK-3β通路的调节作用仍不清楚，需要更多的研究。

目标

探讨GPD1在口腔癌中的调控功能及机制。

结果

结果表明，GPD1 在口腔癌中表达较低。此外，GPD1的过度表达可以减轻口腔癌中的细胞增殖并增强细胞凋亡。 GPD1 的过度表达削弱了口腔癌中的细胞迁移和侵袭。此外，还证实GPD1的过度表达会抑制口腔癌中的线粒体功能。最后说明GPD1触发PI3K/AKT/GSK-3β通路。

结论

该工作首次证明GPD1通过触发PI3K/AKT/GSK-3β通路抑制线粒体功能来抑制口腔癌细胞的增殖、迁移和侵袭。这一发现暗示 GPD1 可能是治疗口腔癌的有用生物标志物。