SLC7A5 (Solute Carrier Family 7 Member 5)

Bone metastasis is an adverse prognostic factor for progression-free survival in lung adenocarcinoma patients treated with third-generation EGFR-TKIs. Bone metastasis lesions exhibit a distinct immunosuppressive tumor microenvironment in EGFR-mutant advanced lung adenocarcinoma, in which upregulation of immune regulatory genes in cancer cells and dysfunction of immune cells may constitute a potential mechanism underlying resistance to third-generation EGFR-TKIs.

Inhibiting this signaling axis in combination with radiotherapy impairs intracranial xenograft growth, resulting in significant survival extensions for treated animals. Overall, our findings uncover a previously unrecognized regulatory axis where PRMT5-mediated R124me2s governs YAP activation through a feedback mechanism, presenting novel therapeutic vulnerabilities in GBM.

Tumor uptake of Cys-PEG5-IR was significantly higher than the unlabeled IR in the subcutaneous MDA-MB-231 TNBC xenograft. This work highlights the prospect of using methionine (Met) transport pathway as an alternative strategy for targeting cancer cells, especially TNBC cells.

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.

Our study established a NM-related gene signature closely linked to immune microenvironment and drug sensitivity, highlighting potential biomarkers and therapeutic targets for prognosis and personalized therapy in HNSCC.

Dioxin-induced carcinogenicity involves intricate AhR-mediated genetic damage and profound epigenetic reprogramming. These alterations, which are often cell-type and species-specific, disrupt critical cellular processes, including EMT and CSC biology, and are susceptible to transgenerational inheritance. The identified molecular signatures offer a foundation for improved biomarkers and targeted therapeutic interventions.

RNA binding protein immunoprecipitation (RIP), RNA pull-down, and actinomycin D (Act D) experiments evaluated fused in sarcoma (FUS)-SLC7A5 interaction...Its expression is transcriptionally driven by FOXM1 and post-transcriptionally stabilized by FUS. Targeting the FOXM1/SLC7A5 axis presents a novel therapeutic strategy for TNBC.

Herein, we analyze the LAT1/SLC7A5-mediated uptake of several essential AAs in FPR2-stimulated CaLu-6 and HCC1937 cells and prove: (i) the redox regulation of both LAT1/SLC7A5 and 4F2hc/SLC3A2/CD98, which form a heterodimer on the plasma membrane; (ii) the redox activation of the mTOR pathway and, in turn, of S6K1 and 4E-BP1, which stimulate protein synthesis; (iii) c-Myc and miR-126 regulation, which control LAT1/SLC7A5 synthesis at the transcriptional and post-transcriptional level, respectively. These findings provide new approaches for the development of novel therapeutic strategies for the treatment of human cancers.

These results suggest that theanine inhibits proliferation in a manner that is still unclear after it is taken up into cells. Based on these findings, we propose that theanine may exert an inhibitory effect on the proliferation of neural cells that have abnormally proliferating Slc38a1, namely neuroblastoma.

Co-inhibition of mTOR or the SLC3A2/SLC7A5 complex using dactolisib or JPH203 restores sensitivity to KRAS inhibitors in vitro and in vivo. These findings support combinatorial targeting of mTOR signaling or amino acid transport to overcome intrinsic resistance in KRAS-mutant lung cancer.

Furthermore, Cy71-Ga NPs can disrupt glutathione synthesis and significantly enhance ferroptosis under laser irradiation. In general, this multimodal theranostic approach includes phototherapy, ferroptosis, chemotherapy of camptothecin, and immunotherapy, achieves an exceptional 83.85% tumor suppression rate in vivo and effectively prevents tumor metastasis.