LIAS (Lipoic Acid Synthetase)

KCNQ1 is a tumor suppressor of CRC that is DNA methylated. DHZCP in combination with KCNQ1 overexpression exhibits anti-CRC effects through the regulation of cuproptosis-related pathways, cuproptosis is promoted, oxidative stress is enhanced, and copper accumulates, thus supporting the clinical application prospects of DHZCP in CRC.

Next, two gastric cancer cell lines (AGS, HGC27) were selected for in vitro experiments to assess the combined effects of PUN and the copper ionophore elesclomol (ES) (hereafter referred to as ES-Cu, representing the combination of ES and Cu2+)...In combination therapy strategies, PUN can work synergistically with chemotherapy drugs to suppress gastric cancer growth. Furthermore, PUN enhances its inhibitory effect on gastric cancer by working synergistically with cuproptosis through targeting FDX1.

The synthetic interaction was conserved across prostate cancer, neuroendocrine tumors, and renal carcinoma cell models, including patient-derived cells, and combined inhibition of FASN and SDH markedly suppressed tumor progression in a breast cancer mouse model. Our findings point to new therapeutic opportunities for FASN inhibition beyond tumor initiation, with particular relevance to cancers associated with malignant SDHB mutations.

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.

DACT1 promotes the malignant behavior of LSCC cells and suppresses cuproptosis by activating the PI3K/AKT signaling.

Combined treatment with an OGT inhibitor OSMI-1 and copper ionophore elesclomol eliminates tumor growth and remarkably enhances the sensitivity of tumor cells to cisplatin. Together, our study identifies TRIM21 Ubiquitinated-ALKBH5 as a critical gatekeeper to restrict cuproptosis, and such mechanism may contribute to tumor development and drug resistance in ESCC.

Here, we report the rational design of CuF16@246, an acid-responsive, dual-functional copper-based nanocoordination polymer that integrates Cu2+ and the p53 reactivator eprenetapopt (APR-246) within a single perfluorosebacic acid (PFSEA)-coordinated framework to synergistically induce cuproptosis and reverse tumor metabolic reprogramming...In vitro and in vivo studies demonstrate that CuF16@246 exhibits more efficient cellular uptake, more potent cytotoxicity, and more significant tumor growth inhibition than individual treatments, without inducing hemolysis or major organ toxicity. This work establishes a dual-functional strategy that combines metabolic reprogramming with sensitized cuproptosis, providing a promising framework for developing advanced copper-based nanomedicines for the treatment of mut-p53-positive cancers.

This further supports the inhibitory effect of thymol on cuproptosis, which underlies its protective properties. This study illustrates that cuproptosis and oxidative stress play crucial roles in the development and progression of cisplatin-induced nephrotoxicity, and the protective activity of thymol is attributed, at least in part, to blunting these mechanisms.

Copper chelators, such as trientine and disulfiram, can regulate intracellular copper levels and induce glioma cell death, thereby enhancing the efficacy of chemotherapy. However, the specific mechanisms of cuproptosis and its clinical application in glioma treatment require further exploration. This field of study promises to offer novel insights and directions for developing more effective glioma therapies.

Our research confirmed that Ce/Cu-modified black ceramics have superior anti-tumor effects and potential mechanisms, confirming the clinical potential of Ce/Cu-modified black ceramics in cancer treatment and providing theoretical basis for the clinical translation.

SIRT7 was recognized as an oncogene in cervical cancer, which boosted cervical cancer cell proliferation and invasion, lowered intracellular copper levels, and prevented cuproptosis. SIRT7 downregulation triggered cuproptosis, inhibiting tumor cell growth.

LIAS promotes cuproptosis and inhibits cancer cell proliferation in PC by activating the p53 signaling pathway to suppress glycolytic activity. These findings indicate that LIAS represents a potential therapeutic target for intervening in PC, and regulation of the glycolysis-cuproptosis axis may serve as an effective strategy for improving PC progression.