LIPT1 (Lipoyltransferase 1)

This inhibition collectively diminishes the expression and activity changes in complex IV, induces mitochondrial dysfunction, and promotes cuproptosis in ovarian cancer. This study further demonstrates that inhibiting the oxidative phosphorylation complex IV can enhance copper-induced cell death in ovarian cancer.

However, on this basis, knocking down EGR1 restored the anti-cancer effect conferred by overexpression of LIPT1. This work aimed to investigate the transcriptional activation of LIPT1 by EGR1 in RCC98 cells to repress the malignant progression of cancer cells while enhancing the sensitivity of RCC98 cells to cuproptosis.

Consequently, LIPT1 deficiency promotes replication and genome instability, and therapeutic vulnerability to PARP inhibitor. Together, these findings reveal a mechanistic link between mitochondrial lipoylation and replication fork stability, uncovering a metabolic basis for genome instability in cancer.

Ferroptosis, cuproptosis, and disulfidptosis each possess distinct advantages and characteristics in the context of melanoma development, metastasis, and drug resistance. Leveraging both their common and unique mechanisms offers new perspectives for improving treatment outcomes.

Finally, knockdown of the SOD2 gene suppressed tumor cell metabolism, proliferation and metastasis. In conclusion, the present study successfully established a prognostic model based on cuproptosis-related mitochondrial genes and developed a nomogram to predict LUAD prognosis with high accuracy, thereby providing improved tools for treatment decision-making and enhancing patient outcomes.

These results provide valuable insights into potential biomarkers and therapeutic targets for BLCA treatment. The CHMP6 protein promotes BLCA cell survival and invasive migration through modulation of the cell cycle.

Importantly, the expression of cuproptosis-related genes was positively correlated with common lymphoid progenitor (CLP) cells and Th2 cells, but negatively associated with NKT cells or Th1 cells. These findings suggest that cuproptosis-related genes are dysregulated across cancer types, hold prognostic value, and may be involved in modulating the tumor immune microenvironment.

Furthermore, mediation analysis identified potential association pathways involving tumor-resident microbes, LM-related gene signatures, and antitumor immune cells. Overall, this study advanced the understanding of the relationship between LM patterns and LUSC tumor biology, as well as its potential clinical implications, which might advance the tailored management of LUSC.

Fluorescence images of colon cancer from different patients demonstrated a positive correlation between CDKN2A expression and the number of CD45+ immune cells. Our research has provided a comprehensive understanding of cuproptosis regulators and revealed potential prognostic biomarkers and therapeutic targets for cancers.

Cuproptosis represents a novel mechanism dependent on copper that has important implications for the treatment of lung cancer. This process primarily involves the buildup of copper ions, which leads to a disruption in protein homeostasis, ultimately resulting in cell death. Additionally, the abnormal expression of crucial regulatory genes, such as FDX1 and LIPT1, along with transport proteins like CTR1 and ATP7A/B, is closely linked to the advancement of lung cancer. At present, drugs that act as carriers for copper ions (such as elesclomol and disulfiram), metal-organic frameworks based on copper, and copper chelators (including D-penicillamine and ammonium tetrathiomolybdate) have demonstrated promise in eliciting copper-mediated cell death in lung cancer cells. These discoveries suggest new potential targets and strategies for treating lung cancer, which could enhance the prognosis for patients diagnosed with the disease.

Five CRGs relevant to pancreatic cancer prognosis were identified. Meanwhile, a new and accurate five CRGs prognostic model of pancreatic cancer was constructed. In addition, LIPT1 may promote proliferation, invasion and migration of pancreatic cancer cell lines. This may have a specific guiding value for future development of precise anti-cancer treatment strategies.