VDAC3 (Voltage Dependent Anion Channel 3)

Specifically, this senescence-like state is driven by PRELID1 and VDAC3 through their cooperative regulation of mitochondria-lysosome interactions in Bgc cells, which enhances IL-7 secretion and promotes functional crosstalk with CD8+ T cells to sustain antitumor immunity. In summary, our findings support a combinatorial strategy integrating targeting of the PRELID1-VDAC3-IL-7 axis in senescence-like Bgc cells with anti-PD-L1 immunotherapy for colorectal cancer.

This ox-LDL-induced upregulation of ACP5 was effectively reversed by the JAK2 inhibitor fedratinib...Conditional ablation of ACP5 significantly reduced aortic plaque area, decreased M1 macrophage proportion in peritoneal lavage fluid, diminished 4-HNE expression in the aortic root, reduced numbers of atrophic mitochondria, and increased aortic GPX4 expression. In conclusion, ACP5 exacerbates atherosclerosis by modulating macrophage polarization and promoting macrophage ferroptosis.

Notably, chloroquine (CQ), an autophagy inhibitor, enhances HPSCC sensitivity to 5-fluorouracil (5-FU), with synergistic effects observed in xenograft models. These findings establish the Trim15-VDAC3-mitophagy axis as a critical regulator of HPSCC progression and chemoresistance, offering a novel therapeutic target for augmenting the efficacy of autophagy inhibitors in combination with standard chemotherapy.

VDAC1 KO specifically reduced glycolytic activity linked to decreased hexokinase localization to mitochondria. These results reveal non-redundant roles of VDAC isoforms in cancer cell metabolic adaptability.

Clinically, the identified ferroptosis-related signatures offer potential as predictive biomarkers for metastatic risk, and ferroptosis induction emerges as a promising therapeutic strategy for metastatic PCa. Future research should focus on exploring the crosstalk between ferroptosis and other cancer-related pathways to develop more effective targeted therapies.

This study integrates bioinformatic insights with experimental validation to clarify the clinical significance and therapeutic potential of VDACs in LUAD, providing a valuable foundation for prognosis assessment and targeted therapy development.

On the other hand, tubulin antagonists like erastin induce VDAC1/2 opening to reverse the Warburg effect, killing cancer cells via ferroptosis, and its oligomerization state can reverse apoptotic resistance. Advances in targeted therapy show that compounds based on VDAC gating regulation (such as avicin/acrolein for channel closure and erastin/betulinic acid for channel opening) exhibit significant antitumor effects in models of lung cancer, breast cancer, etc. Moreover, the interaction between TSPO and VDAC, as well as oligomerization regulation mediated by GPCPD1, have emerged as novel strategies.This review highlights the functional heterogeneity of VDAC isoforms and the challenges posed by ROS concentration thresholds for precision therapy, providing a theoretical basis for developing cancer treatment strategies targeting mitochondrial channels.

The formation of intermolecular disulfide bonds helps to explain the previously observed VDAC oligomerization and demonstrates that disulfide bridges are directly involved in their homo- or hetero-oligomerization. Data are available via ProteomeXchange with identifier PXD064110.

VDAC1 KO specifically reduced glycolytic activity linked to decreased hexokinase localization to mitochondria. These results reveal non-redundant roles of VDAC isoforms in cancer cell metabolic adaptability.

Finally, analysis of the CellMiner database predicted that VDAC3 expression was positively correlated with chelerythrine and cladribine, but negatively correlated with Ergenyl. Our study suggests that VDAC3 may be a potential biomarker for early diagnosis, prognosis, and treatment of COAD.

This finding reveals the molecular mechanisms underlying T-DXd resistance in HER2-low breast cancer. Our study provides a new strategy to overcome T-DXd resistance by inhibiting the interaction between crVDAC3 and HSPB1 protein.

In addition to the previous findings, these results significantly extend the characterization of the oxidation state of cysteines in rVDAC2 and show that it is highly complex and presents unusual features. Data are available via ProteomeXchange with the identifier PXD044041.