SLC3A2 (Solute Carrier Family 3 Member 2)

In vivo, rAGR2 accelerated tumor growth in melanoma and lung cancer models, accompanied by increased TAM accumulation, a shift toward M2 polarization, and suppressed T-cell function. AGR2 drives tumor progression by reprogramming TAMs toward an M2 phenotype and attenuating T-cell function via the CD98hc-xCT/p-ERK pathway, highlighting its potential as both a prognostic marker and a therapeutic target.

In this review, we discuss recent advances in understanding the structure, expression, and regulatory mechanisms of SLC7A7, focusing on its role in cancer development and the current research limitations. Furthermore, this review emphasizes the role of SLC7A7 in promoting cancer immune escape by influencing innate and adaptive immune cells in the TME and discusses its potential mechanisms of immune cell regulation.

NRG1 fusions were identified in 0.8% of NSCLC, exceeding historical estimates and underscoring the importance of RNA-based NGS for fusion detection. The clinical and molecular profile mirrored prior reports, with predominant female patients, IMA histology, PD-L1 negativity, and low TMB. Outcomes were poor in metastatic patients lacking access to targeted therapy, supporting the need for broader implementation of RNA sequencing and access to anti-HER3 agents.

Molecular docking confirmed that LT4 stably occupied the ATP‑binding pocket of PI3Kγ with a binding energy comparable to wortmannin and a conformation similar to antroquinonol. In conclusion, to the best of our knowledge, the present study is the first to comprehensively demonstrate the multi‑target anti‑CRC effects of LT4, highlighting its potential as a therapeutic agent, especially in KRAS‑mutant CRC.

NFIB knockout enhances erastin-induced ferroptosis, marked by elevated Fe2 +, MDA, and ROS levels...In vivo, combined NFIB suppression and ferroptosis induction significantly inhibit tumor growth and increase lipid peroxidation in CRPC xenografts. These findings uncover a critical role of NFIB phase separation and acetylation in ferroptosis regulation and suggest NFIB as a promising therapeutic target in CRPC.

Collectively, these findings establish SLC3A2 as playing a vital oncogenic role in BC tumorigenesis and progression. Its function in inhibiting ferroptosis-especially during cisplatin-based chemotherapy-makes it a promising therapeutic target.

This process enhances SLC3A2 protein stability by thwarting its degradation, culminating in acquired gemcitabine resistance. This study unveils a novel mechanism of gemcitabine resistance in pancreatic cancer and provides a potential therapeutic target for reversing drug resistance.

Plasma cell-specific deletion of Myd88 led to reduced survival and antibody secretion by antigen-specific cells in vivo and unresponsiveness to BAFF and APRIL ex vivo. These data reveal novel regulators that link plasma cell secretory capacity and lifespan.

Genetic variants in ASCT2 and LAT1-related genes are independently associated with survival in CRC, supporting the growing body of evidence supporting personalized medicine and highlighting the need to consider both genetic and tumor heterogeneity when defining risk and tailoring treatment strategies.

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.

Taken together, this study leverages LLM-guided discovery to delineate a novel ALKBH5/CHRM3/ZNF281 regulatory axis controlling ferroptotic susceptibility in PCa. Importantly, a synergistic therapeutic strategy was identified by combining RSL3 with AZD5363, providing novel therapeutic targets and directions for PCa treatment.

LRP8 facilitates CRC progression by antagonizing ferroptosis via modulation of the SLC3A2/GPX4 signalling axis. These findings highlight LRP8 as a previously unrecognized regulator of ferroptotic vulnerability and a potential therapeutic target in CRC.