SLC7A11 expression

Importantly, the system xc- inhibitor Sorafenib or Imidazole ketone erastin effectively inhibited the growth of tamoxifen-resistant breast cells in vitro and in vivo. In conclusion, our data reveal that targeting estrogen-regulated SLC7A11 and SLC3A2 enhances ferroptosis in ER+ breast cancer, offering a novel therapeutic option for patients with ER+ breast cancer, particularly those with endocrine resistance.

However, anlotinib-induced ferroptosis was suppressed in p53-deficient cells. Collectively, these findings confirm that anlotinib exerts potent anti-tumor effects both in vitro and in vivo by inducing ferroptosis by modulating the p53/xCT/GPX4 pathway specifically within NSCLC cells.

What is more, our study demonstrated that sorafenib had the capability to enhance the MHC-I antigen presentation process, thereby facilitating T cell-mediated killing of NPC cells via targeting SLC7A11. Consequently, targeting SLC7A11 with sorafenib emerges as a promising therapeutic strategy for the treatment of NPC.

The high expression of SLC7A11 may indicate a high recurrence rate for ISMC. Immunotherapy with checkpoint inhibitors and iron death-related treatments show potential in the treatment of ISMC, with SLC7A11, SLC3A2, and PD-L1 serving as potential therapeutic targets for ISMC.

METTL3 regulated the transcription of SLC7A11 through GATA3 and KDM6B to modulate ferroptosis in an m6A-dependent manner. This study provides a novel potential strategy and experimental support for the future treatment of cancer.

In conclusion, our study suggests that METTL3 regulates the stability of SLC7A11 mRNA in an m6A/IGF2BP2-dependent manner and the ubiquitination of SLC7A11 protein through the m6A/YTHDF2/SOCS2 pathway, both of which require the m6A methyltransferase activity of METTL3. METTL3 or IGF2BP2 may be promising targets for radiotherapy of HCC.

SLC7A11 suppresses pyroptosis to alleviate RA development by inhibiting the IL-17 pathway.

In vivo experiments demonstrated that the ASIC1a-specific inhibitor PcTx-1 ameliorated histopathological characteristics of ankle joints in collagen-induced arthritis (CIA) mice, decreased p53 expression, and enhanced NRF2 and SLC7A11 expression in chondrocytes. These findings suggest that ASIC1a inhibition may mitigate acidification-induced ferroptosis in articular chondrocytes in RA, potentially via the p53/NRF2/SLC7A11 pathway.

Finally, our results showed that F. nucleatum and its metabolic derivates promote tumor spheroids growth, spheroids-derived cell detachment, epithelial-mesenchymal transition and Galectin-9 upregulation. Altogether, F. nucleatum promotes pro-tumoral mechanism in oral cancer.

SLC7A11/xCT is a poor prognostic marker for liver cancer and is mainly expressed in DCs in the TME. Targeting xCT in DCs combined with RFA significantly enhances anti-tumor immunity, suppressing tumor growth and offering a promising strategy for improved therapeutic outcomes in liver cancer.

This study provides mechanistic insights into sevoflurane-induced neurotoxicity, emphasising the importance of SLC7A11 in regulating astrocyte ferroptosis. Our findings highlight the potential for targeting ferroptosis pathways to mitigate the adverse effects of sevoflurane anaesthesia.

The depletion of PRKAA2 enhanced the erastin-induced inhibition effect on cell growth, and notably increased the levels of MDA, ROS, iron, and Fe2+, while decreased GSH level in NSCLC cells...The results discovered that PRKAA2 accelerated the malignant progression, diminished apoptosis and ferroptosis in NSCLC through SLC7A11/GSH/GPX4 pathway. This study provide a novel target in the application of PRKAA2 for NSCLC treatment.