Department of Emergency and Critical Disease, Songjiang Research Institute, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 201600, China; Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Gene. 2025 Jan 15;933:148976. doi: 10.1016/j.gene.2024.148976. Epub 2024 Oct 1.
Mitochondria are essential for cell metabolism and survival as they produce the majority of cellular ATP through oxidative phosphorylation as well as regulate critical processes such as cell proliferation and apoptosis. NIPSNAP family of proteins are predominantly mitochondrial matrix proteins. However, the molecular and cellular functions of the NIPSNAPs, particularly NIPSNAP3A, have remained elusive. Here, we demonstrated that NIPSNAP3A knockdown in HeLa cells inhibited their proliferation and migration and attenuated apoptosis induced by Actinomycin D (Act-D). These findings suggested a complex relationship between cellular processes and mitochondrial functions, mediated by NIPSNAP3A. Further investigations revealed that NIPSNAP3A knockdown not only inhibited mitochondrial fission through reduction of DRP1-S616, but also suppressed cytochrome c release in apoptosis. Collectively, our findings highlight the critical role of NIPSNAP3A in coordinating cellular processes, likely through its influence on mitochondrial dynamics.
线粒体对于细胞代谢和生存至关重要，因为它们通过氧化磷酸化产生大部分细胞 ATP，并且调节细胞增殖和凋亡等关键过程。NIPSNAP 蛋白家族主要是线粒体基质蛋白。然而，NIPSNAP 的分子和细胞功能，特别是 NIPSNAP3A，仍然难以捉摸。在这里，我们证明了在 HeLa 细胞中敲低 NIPSNAP3A 会抑制其增殖和迁移，并减弱 Actinomycin D（Act-D）诱导的细胞凋亡。这些发现表明，细胞过程和线粒体功能之间存在复杂的关系，由 NIPSNAP3A 介导。进一步的研究表明，NIPSNAP3A 敲低不仅通过减少 DRP1-S616 抑制线粒体分裂，而且在细胞凋亡中抑制细胞色素 c 的释放。总的来说，我们的研究结果强调了 NIPSNAP3A 在协调细胞过程中的关键作用，可能通过其对线粒体动力学的影响。
