Herein, a metabolic-interfering PtIV complex DPR was constructed by anchoring a cyclic peptide (RGDfK)c and dichloroacetate (DCA) at the axial positions of cisplatin. Notably, DPR achieved remarkable antitumor efficacy with minimal systemic toxicity in a GL261-bearing mouse model. This study highlights DPR as a promising GBM-target PtIV complex that exerts therapeutic effects by synergistically interfering with energy metabolism and inducing ferroptosis, providing an innovative strategy to overcome therapeutic resistance in GBM.

For peptide analysis, ANALLANGVELR (AR-12) and VVNLLSAIK (VK-9) were chosen as specific peptides...In addition, application data for reagents certified by these methods in cell apoptosis assays and kit evaluation are provided: TNF-α-induced cell apoptosis was significantly attenuated by antagonists, while detection kits based on three different principles exhibited good repeatability (RSD 0.999). This accurate, SI-traceable method can improve clinical TNF-α assay standardization and biomarker reliability.

Furthermore, we identify sodium 2, 2-dichloroacetate (DCA) as a novel inhibitor of USP30, and DCA inhibits CRC serine synthesis and tumor growth. Clinically, USP30, FTO, PHGDH, and PSAT1 levels are highly correlated in CRC tissues. This study provides mechanistic insights into how USP30 senses serine/glycine levels to regulate serine synthesis via the FTO-PHGDH/PSAT1 axis, offering a potential therapeutic strategy for targeting serine/glycine metabolism in cancer.

This study aimed to investigate the effectiveness of sodium dichloroacetate (NaDCA) and a sodium valproate NaDCA combination (NaVPA-NaDCA) on formed patients' primary cell tumors on the chick embryo chorioallantoic membrane (CAM). The treatment with NaVPA-NaDCA significantly reduced the expression of PCNA, p53, EZH2 and vimentin in the tested tumors. Data demonstrated an antitumor effect of NaVPA-NaDCA in an in vivo model of a patient's primary glioblastoma cells.

NKILA facilitated proliferation, invasion, Warburg effects, and autophagy of ICC cells by regulating mammalian target of rapamycin (mTOR) pathway, PD-L1 expression, and CD8+ T cytotoxicity, while dichloroacetate (DCA) could reverse these effects...NKILA silencing could inactivate MTX1/TOMM40 axis to inhibit Warburg effect and autophagy-associated immune escape. LncRNA NKILA promotes Warburg effect and immune escape in ICC by regulating the MTX1/TOMM40 axis.

Lactate drives H3K18la-mediated transcriptional activation of IGF2BP2 in CRC. IGF2BP2 protein stabilises Nrf2 mRNA by binding to its m6A modification site. The lactate-IGF2BP2-Nrf2 axis confers ferroptosis resistance in CRC cells. This pathway simultaneously promotes M2 macrophage polarisation in the tumour microenvironment.

DCA amplified PDT-induced oxidative stress, overcoming redox defenses and enhancing ferroptotic and immunogenic responses. These findings suggest that combining DCA with PDT enhances multimodal cell death in PDAC, providing a rationale for further in vivo studies to validate this redox-metabolic approach to treating chemoresistant pancreatic tumors.

In this study, 20 new derivatives were designed and synthesized through further structural optimization of the dichloroacetate (DCA) derivatives, and their inhibitory effects on PDK1 and anticancer activities were systematically evaluated...Importantly, low-dose D16 (20 mg/kg) robustly inhibited tumor growth in vivo without systemic toxicity. These findings establish D16 as a potent PDK1 inhibitor that shifts tumor metabolism, offering a promising therapeutic approach for cancer treatment.

Furthermore, predictive modeling and molecular docking revealed that tumors with elevated CENPW levels exhibited enhanced sensitivity to targeted therapies such as OSU-03012 and rapamycin. Collectively, our findings indicate that CENPW acts as a potential oncogenic regulator in KIRC, influencing both immune pathways and therapeutic responsiveness, and may serve as a novel biomarker and treatment target.

2 mM NaVPA-3 mM NaDCA, as well as temozolomide, had individual impacts on the SLC12A2, SLC12A5, CDH1, CDH2, EZH2, and GFAP expressions of tested GBM5-1, GBM5-2F, and GBM5-3F primary cells of female GBM patients. The combination of 2 mM NaVPA-3 mM NaDCA may have an advantage in antitumor activity and may be more effective than TMZ; however, the effect is individual.

The findings suggest PDK1 as a critical regulator of glycolytic metabolism and a potential therapeutic target in osteosarcoma. Targeting PDK1 could provide a novel therapeutic strategy for treating osteosarcoma and possibly other cancers.

It is well-established that pyruvate dehydrogenase kinase (PDK)-mediated phosphorylation of PDH leads to its inactivation and that dichloroacetic acid (DCA), a PDK inhibitor, has been investigated in preclinical and early clinical studies as a potential therapeutic agent for lung cancer. This study aims to elucidate how PLK1-associated activity drives the metabolic reprogramming from OXPHOS to glycolysis during cellular transformation, thereby contributing to lung carcinogenesis. Our results provide support for a clinical trial to evaluate the efficacy of Onvansertib plus DCA in treating lung cancer.