SLC2A1 (Solute Carrier Family 2 Member 1)

TSZAF mc inhibits ovarian cancer progression by regulating the AKT/ FOXO3A-mediated glycolysis pathway, which may represent one of the mechanisms underlying the clinical efficacy of TSZAF in ovarian cancer treatment.

RNase R digestion and actinomycin D assays were employed to assess its stability...Animal experiments confirmed that silencing circ_0017521 suppressed tumor growth and glycolysis. This study revealed that hypoxia-induced circ_0017521 activated the PI3K/AKT pathway through the miR-532-3p/PFKFB3 axis, synergistically driving EMT and glycolysis, thereby promoting NSCLC progression.

Importantly, targeting GLUT1 pharmacologically partially reverses the proliferative advantage conferred by ETV6 overexpression, highlighting a promising therapeutic vulnerability. Our findings establish the FBXW7-ETV6-GLUT1 regulatory axis as a critical driver of metabolic adaptation and tumor progression, offering potential strategies for targeted therapy in FBXW7-mutant EC.

Compared with normal brain tissue, glioma tissue exhibited significantly elevated glucose transporter type 1 protein levels. In conclusion, the model was confirmed by high‑resolution small animal PET‑CT and MRI, as well as morphological and pathological approaches.

FKBPL-based peptide mimetic, AD-01 (1 nM), in high-glucose conditions, upregulated endothelial vcam1 and glut1 mRNA expression, independent of miR-302b-5p. FKBPL plays an important role in glucose metabolism, endothelial function, angiogenesis, cardiac inflammation and function, and could be explored as a therapeutic target of cardiovascular disease both in nondiabetes and diabetes settings using precision medicine approach.

The expression levels of PI3K, p-AKT/AKT proteins, and Ki67 were significantly lower in the TNKS1-siRNA group, inhibitor group, and TNKS1-siRNA + inhibitor group. TNKS1 regulates glycolysis and proliferation in glioma by mediating the PTEN-PI3K/AKT pathway.

In vitro cytotoxicity evaluation was performed using the MTT assay on HCT116, LOVO, CT26.WT cell lines. Following in vivo evaluations of biodistribution, anti-tumor efficacy, and biosafety in CT26.WT xenograft tumor-bearing mice, PSSQ@TLP demonstrated enhanced intratumoral accumulation, robust tumor suppression, and minimized systemic toxicity, underscoring its promise as a targeted therapeutic strategy for colorectal cancer.

Cryoablation is an effective treatment for OMM, and its antitumor effects are potentially linked to the modulation of the immune microenvironment, alteration of glucose metabolism, and induction of apoptosis.

Prostratin, a non-tumorigenic phorbol ester, activates aPKC and induces a similar effect on intestinal glucose excretion. We identify the prostratin and aPKC/GLUT1 signalling pathways as putative targets for treating diabetes, providing insights into the future development of antidiabetic and weight-loss drugs.

Collectively, our findings reveal that the USP20-RAB8A-GLUT1 axis regulates glucose uptake and metabolic reprogramming in PDAC, thereby inhibiting tumor growth and metastasis. Targeting this signaling axis provides a novel insight into metabolic therapy for pancreatic cancer.

Particularly, we found overexpression of GLUT1, FLIP and downregulation of BAX, BAK, MLKL and CDX2 proteins in the cancer stem cell of early recurrence samples.We built a neural network based on the cancer stem cell protein signature (BAX, MLKL, FLIP, GLUT1 and CDX2 proteins) that delivers a high-performance prognostic classifier.How this study might affect research, practice or policy: Our results propose a clinically promising prognostic tool based on a five-protein stem cell signature that outperforms existing clinical and proposed transcriptomic based signatures for separation between risk groups.Moreover, our five-protein signature markers not only predict stem cell chemotherapy resistance and therefore tumour recurrence but also suggest potential therapeutic strategies. For instance, this approach could guide combinatorial treatments at high risk of chemoresistance, such as incorporating small molecule inhibitors targeting FLIP (currently in discovery phase) and GLUT1 (already under preclinical trial evaluation).

YQJDF inhibits proliferation, invasion, and migration of NPC cells by inhibiting the AKT1/GLUT1 signaling pathway.