SLC1A5 (Solute Carrier Family 1 Member 5)

As a proof-of-concept, we develop a nanoplatform for ferroptosis named MICLM, which is obtained by encapsulating chlorin e6 (Ce6, a photosensitizer) and IMD-0354 (an SLC1A5 inhibitor) into metal-organic framework (NH2-MIL-101(Fe)), followed by surface coating for tumor-targeting. Additionally, Gln metabolism inhibition attenuates immunosuppressive M2 macrophage polarization, ultimately boosting antitumor immunity. Thus, MICLM effectively induces ferroptosis and remodels the tumor immune microenvironment via amino acid metabolic intervention, offering a promising strategy for ferroptosis-based therapy.

This study suggests that SLC1A5 is upregulated in TEX, which modulates kynurenine metabolism and induces T cell exhaustion through the AHR-FANCD2 axis-mediated chromatin remodeling.

Our data demonstrate that the enhanced MTFP1 expression leads to an upregulated glutamine-OXPHOS axis in PDAC liver colonisation. This metabolic shift is triggered by the ROS/PI3K/AKT/c-MYC/SLC1A5 pathway. Targeting MTFP1 may be a potential therapeutic strategy for PDAC patients with liver metastasis.

Together, these findings establish ACTL8 as a key oncogenic driver of BC progression. Targeting ACTL8 offers a novel strategy to disrupt glutamine-dependent metabolic reprogramming, and Momordin Ic represents a promising lead agent to combat ACTL8-driven BC.

Rescue experiments used N-acetylcysteine (NAC) and chloroquine (CQ)...CQ but not MG-132 increased CD276 expression in ESCC cells...SLC1A5 enhances CD276 stability by suppressing ROS-autophagy signaling, promoting ESCC progression. Targeting glutamine metabolism to enhance CD276 degradation might be a novel therapeutic strategy for ESCC.

Finally, we also documented an increase in mitochondria reactive oxygen species (mtROS). The combined inhibition of SIRT3 and activation of SIRT5 greatly reduces the size of spheroids through the inhibition of hypoxic response, which is then followed by the alteration of the autophagic and mitophagic process and the toxic accumulation of mitochondrial ROS, representing a new anti-tumoral strategy.

According to the FRG model, individuals classified as low-risk exhibited more favorable survival prospects compared to their high-risk counterparts (P < .05). Overall, our investigation highlights the promise of FRGs as prognostic biomarkers and immunotherapy response in HCC, providing a novel approach for personalized patient management.

Our findings suggest that SS is a glutamine-dependent malignancy and validate ASCT2 as a promising therapeutic target. The ASCT2 inhibitor V9302 demonstrated therapeutic efficacy both in vitro and in vivo, supporting its potential as a therapeutic agent for SS.

Selective inhibitors like BAY-876 show preclinical efficacy. Combining SLC inhibition with standard therapies may overcome resistance, while personalized strategies and advances in biomarkers and drug delivery are critical for clinical translation.

In humans, microbiota-encoded genes contributing to aa depletion are associated with colorectal cancer progression. Collectively, these findings reveal nutrient-dependent modulation of anticancer immunity by the gut microbiota and identify diet-microbiota-cancer crosstalk as a potential therapeutic target.

Biomarkers such as xCT/GPX4 expression, PHGDH levels, Nrf2 activity, and GSH/NADPH ratios may guide patient stratification and response prediction. Overall, understanding the redox-amino acid metabolic network provides a mechanistic basis and translational opportunities for precision metabolic therapies in ovarian cancer.