SLC7A2 (Solute Carrier Family 7 Member 2)

Additionally, arginine uptake could effectively alleviate oxidative stress and reduce cell apoptosis via the synthesis of glutathione (GSH) and the activation of NRF2/HO-1 signaling upon ASCT2 knockdown. These results not only delineate the metabolic reprogramming cascade mediated through ASCT2 suppression, but more importantly, reveal a clinically actionable strategy of dual glutamine-arginine metabolic intervention with translational promise for overcoming therapy resistance across multiple pathological states, particularly in malignancies exhibiting metabolic plasticity.

FGD5-AS1 sponged miR-195-5p to mediate the upregulation of SLC7A2, overexpression of which promoted aggressiveness of OS cells. In summary, METTL16-mediated upregulation of FGD5-AS1 promotes the aggressiveness of OS though targeting of miR-195-5p/SLC7A2 axis.

This study provides new insights into prognostic prediction and immunotherapy for STAD from the perspective of the inflammatory response.

We developed an OFRG-related signature to predict the prognosis and treatment responsiveness of individuals with GC and identified CDH19 as a possible therapeutic target for GC.

It is concluded that SLC7A2 is involved in HNSCC lymphatic metastasis by controlling CPB2 function. The results are anticipated to offer new directions for the effective treatment of HNSCC.

Predictive risk score based on 8 ERGs exhibited excellent prognostic value in UCEC patients, and high-risk patients had inferior survival. UCEC patients with distinct prognoses showed different tumor immune microenvironment.

Additionally, overexpression of SLC7A2 activates CD8+ T cells and enhances the chemosensitivity of anti-PD-1 therapies in vivo. In conclusion, SLC7A2 may function as an antitumor gene in TNBC by activating antitumor immunity, suggesting SLC7A2/ACOX1/TCF1 signaling as a promising therapeutic strategy.

We constructed a six-gene BM-related prognostic model for predicting GC prognosis, immune cell infiltration, TMB status, and chemotherapy response. This research provides new ideas for developing more effective individualized treatment of GC patients.

A lysine-restricted diet synergized with MYC inhibition or anti-PD-1 therapy to slow tumour growth. Collectively, GSCs co-opt lysine uptake and degradation to shunt the production of crotonyl-CoA, remodelling the chromatin landscape to evade interferon-induced intrinsic effects on GSC maintenance and extrinsic effects on immune response.

Furthermore, CCL20 knockdown combined with SLC7A2 overexpression availably weakened the tumor growth in vivo. Collectively, IRG score, serving as a potential candidate, accurately and stably predicted the prognosis and response to immunotherapy in virus-related HCC patients, which could guide individualized treatment decision-making for the sufferers.

Further studies revealed that RIOK3 promoted arginine uptake, mechanistic target of rapamycin complex 1 (mTORC1) activation, cell invasion, and metastasis in PDAC cells via SLC7A2. Finally, we found that patients with high expression of both RIOK3 and infiltrating Treg cells had a worse prognosis. Overall, our study found that RIOK3 in PDAC cells promotes arginine uptake and mTORC1 activation through upregulation of SLC7A2 expression, and also provides a new therapeutic target for therapeutic strategies targeting arginine metabolism.

SLC7A2 and CGB3 were downregulated with ALKBH5 knockdown. In this study, we found that ALKBH5 might be a suppressor of GC; ALKBH5 and its related genes were latent biomarkers and immunotherapy targets.