Slc25a43, encoding a mitochondrial transport protein, is involved in mitochondrial function and associated with cell cycle regulation, metabolism, and oxidative stress response pathways [2,3,4,5,6]. Its study using genetic models has been crucial in deciphering its biological importance.

Knockout (KO) of Slc25a43 in mouse embryonic stem cells (ESCs) led to reduced damage caused by reactive oxygen species (ROS) and higher cell viability when exposed to H₂O₂. This indicates that Slc25a43 is a main target gene of oxidative toxicity, and its KO activates mitochondria-related genes like Nlrx1 to protect ESCs from oxidative damage [1].

In breast epithelial cells, suppressing SLC25A43 expression using siRNA affected cell cycle progression. In non-cancerous MCF10A cells, it inhibited G1-to-S transition, reducing the proliferation rate, while in HER2-positive breast cancer BT-474 cells, it enhanced G1-to-S transition and increased the proliferation rate [2]. In breast cancer cell lines, knockdown of SLC25A43 decreased the cytotoxic effect of paclitaxel and trastuzumab, and also affected cell cycle arrest induced by these drugs [5].

In conclusion, Slc25a43 plays a significant role in mitochondrial-related biological processes such as oxidative stress response and cell cycle regulation. Gene knockout models have revealed its importance in diseases like breast cancer, providing insights into the underlying mechanisms and potential therapeutic targets related to mitochondrial function and cell cycle dysregulation in cancer [1,2,5].