SLC1A3 (Solute Carrier Family 1 Member 3)

Notably, glutamate depletion enhances the efficacy of neoadjuvant immunochemotherapy. Our findings provide insights into how the METTL3/m6A/CD98 axis-mediated regulation of glutamate efflux may sensitize HNSCC to neoadjuvant immunochemotherapy.

JPJDF suppresses CRC metastasis by targeting glutamine metabolism via the YTHDF1/GID8 axis and by remodeling the immunosuppressive tumor microenvironment, highlighting its potential as an adjunct therapeutic strategy for metastatic CRC.

124 T thus effectively detargets endogenous neurons, refining target cell specificity, while further guiding reprogramming outcomes. This approach establishes a foundation for precision reprogramming platforms aimed at restoring specific neural cell types.

Our results revealed significant associations between amino acid metabolism gene polymorphisms and PTC risk, suggesting potential biomarkers for PTC susceptibility.

This study elucidates the synergistic mechanisms and identifies key resistance pathways underlying chemo-immunotherapy combinations in patients with ESCC, providing a scientific basis for refining future combination therapeutic regimens.

Suppression of SENP5 slows the development of ESCC by inhibiting the NF-κB‒SLC1A3 axis through SUMO1-mediated SUMOylation of IκBα. Our research suggests that SENP5 could serve as a prognostic indicator and a target for therapeutic intervention for ESCC patients.

High expression of SLC1A3 is linked to poor prognosis in ovarian cancer patients. SLC1A3 activity impedes apoptosis while enhancing the proliferation and migration of ovarian cancer cells, suggesting its potential as a therapeutic target for drug development.

SLC1A3 functions as a cancer-promoting factor contributing to poor HCC prognosis by affecting immune cell infiltration and regulating the EMT process. Elevated SLC1A3 expression may also serve as a predictor of treatment response to specific antitumor drugs.

Finally, CPS1 overexpressing adeno-associated virus can dampen HCC progression. Collectively, this results uncovered that CPS1 is a switch between HCC proliferation and metastasis by increasing intracellular aspartate level.

In contrast, pre-ciliated cells (Krt5+, Prom1+, Trp73+) remain cancer-prone and give rise to serous tubal intraepithelial carcinomas and overt HGSC. These findings identify transitional pre-ciliated cells as a cancer-prone cell state and point to pre-ciliation mechanisms as diagnostic and therapeutic targets.

Inhibition of GID8 attenuated CRC proliferation and metastasis both in vitro and in vivo. In summary, we identified a previously unknown target pertaining to glutamine uptake and metabolism in tumor cells, underscoring the potential of GID8 in the treatment of CRC.