HK2 (Hexokinase 2)

The observed reductions in tumor burden and key biomarkers corroborate the therapeutic potential of this approach. Collectively, these preclinical findings suggest that electroacupuncture and moxibustion, as non-pharmacological adjunctive therapies, hold translational potential for modulating tumor metabolism and slowing HCC progression, warranting further clinical investigation.

In vivo, high glucose synergized with PKA activation to promote metastasis, whereas glycolysis inhibition blocked new metastases. Thus, HHEX-PRKAR2B-mediated PKA activation is a critical hub for PDAC progression, modulated by glucose and reinforcing glycolysis via HK2, revealing novel therapeutic targets for metabolic intervention.

This study identifies S100A10 as a critical oncogenic driver in CCA that links metabolic reprogramming to tumor progression via the HK2/ERK signaling axis. These findings suggest S100A10 is a robust prognostic biomarker and a potential therapeutic target for disrupting the metabolic adaptability of cholangiocarcinoma.

NAT10-mediated ac4C modification is a critical regulatory node integrating tumor immunity and metabolism, serving as a promising potential target for precision cancer therapy. Current research still faces challenges such as insufficient sensitivity and specificity of ac4C detection technologies, unclearcell-type-specific mechanisms of NAT10, limited delivery efficiency of inhibitors, and the existence of compensatory pathways. Future research should focus on optimizing ac4C detection technologies, clarifying cell-type-specific mechanisms, developing targeted delivery systems, and further exploring the clinical translational value of combining NAT10-targeted therapy with immune checkpoint blockade, so as to provide new strategies and technical support for cancer treatment.

We find that bedaquiline (ATP synthase inhibitor) outperforms oligomycin A in specificity, VLX600 (electron transport chain inhibitor) shows superior selectivity to rotenone/metformin, and CPI-613 (tricarboxylic acid cycle blocker) surpasses other glutaminase inhibitors. MitoATP-nFCM establishes a quantitative single-organelle platform that profiles elevated mitoATP levels in cancer cells and enables precision screening of OXPHOS-targeting inhibitors.

Cop ameliorates IR by targeting SMARCE1-mediated suppression of glycolytic flux. These findings elucidate both the mechanistic basis and therapeutic potential of Cop for the treatment of metabolic disorders.

Nitrosative stress can promote the malignant biological behavior of breast cancer cells through the glycolytic pathway.

Dox resistance in DLBCL was mediated by P300-facilitated glycolysis.

Our multi-omics approach reveals coordinated dysregulation of glucose metabolism and inflammatory genes following ICH, with time-dependent HK2 regulation in microglia and synchronized transcriptional changes at day 7 representing critical events in neuroinflammatory progression. The identified gene networks and cellular communication patterns provide new insights into the metabolic-immune interface in ICH, offering potential targets for future therapeutic strategies.

Collectively, our findings demonstrate that ZNF454 suppresses CRC development by inhibiting FSTL3/HIF-1α-mediated glycolysis through transcriptional repression of FSTL3. This study is the first to reveal the molecular mechanism responsible for FSTL3 overexpression in CRC, providing a novel perspective for CRC treatment.

This article systematically reviews the regulatory effects of curcumin on these critical metabolic processes and pathways in tumor metabolic reprogramming, revealing its molecular mechanisms in disrupting tumor growth and progression by targeting energy and biosynthetic metabolism. These findings provide a significant theoretical foundation and a preclinical research perspective for the development of natural antitumor drugs based on metabolic regulation, as well as for optimizing combination therapy strategies.

While monotherapies often fail due to compensatory pathways and drug resistance, dual-targeting both HK2 and its regulatory miRNAs could achieve substantial metabolic inhibition. This review summarizes recent advances in miRNA-HK2 regulatory networks across cancers and highlights dual-targeting miRNA-HK2 as a promising therapeutic strategy to overcome metabolic plasticity and improve precision, durability, and efficacy in cancer therapy.