SLC1A2 (Solute Carrier Family 1 Member 2)

These findings advance the concept of 'differentiation therapy' as a promising intervention to reduce phenotypic plasticity and malignancy in pHGG ecosystems. While these are early in vitro findings, the potential ability to steer and control glioma cells toward stable, less malignant fates offers promising translational potential for patient-centered targeted therapies.

We identified an 11-gene prognostic signature, including SPP1 and SLC2A1 associated with poor prognosis, and genes such as ITGAM and P2RY6 predictive of immunotherapy response. These findings provide insights into the chemokine-immune-metabolic network and support further validation toward personalized HCC treatment.

We demonstrate distinct morphology of TAAs and different roles in various regions of the tumor. Glioma-induced heterogeneity of TAAs allows adaptation to the pharmacologically induced modification of the immunosuppressive TME.

Taken together, these findings suggest that ACR induces neuronal excitotoxicity by interfering with astrocytic EAAT2-mediated regulation of extracellular glutamate, leading to extrasynaptic NMDAR overactivation, intracellular calcium overload, and Tau-related neurodegeneration. The EAAT2 is a potential therapeutic target for mitigating ACR-induced neurotoxicity and associated sequelae such as cognitive impairment.

This study investigated whether CD44-SLC1A2 gene fusions, reported in gastrointestinal malignancies, contribute to ET resistance mechanisms in breast cancer. Although no CD44-SLC1A2 fusions were detected, high expression of CD44 and SLC1A2 was associated with poor survival outcomes and identified a therapy-resistant subpopulation sustained by aspartate and glutamate metabolism, highlighting potential metabolic vulnerabilities for future therapeutic intervention.

miR-199b-5p targets solute carrier transporters (SLC1A2/EAAT2 in astrocytes and SLC38A2/SNAT2 and SLC16A7/MCT2 in neurons) to hijack the neuron-astrocyte metabolic coupling, leading to extracellular retention of these metabolites and promoting cancer cell growth. Our findings reveal a mechanism through which cancer cells of a non-brain origin reprogram neural metabolism to fuel brain metastases.

The retained expression of pyruvate carboxylase may contribute to determining a pathological glutamate excess unopposed by glutamine synthetase that resulted expressed to a variable extent in the majority of the tumors. Furthermore, we can assume that the EAAT2 loss in brain tumors in general and in LEATs in particular is more conceivably epigenetic.