Congratulations! Great work👏🏻👏🏻

Special thanks to dream team spearheaded by Vittoria Graziani and Eva Crosas-Molist; all co-authors and collaborators. Thanks to all the funders that supported us and @cp-cellreports.bsky.social for such a constructive review process!

5. Targeting SLC7A11 offers a therapeutic opportunity for patients with SLC7A11-high tumours. SLC7A11 could also serve as a biomarker for invasive phenotypes, aiding patient stratification and precision oncology approaches.

4. Erastin-mediated SLC7A11 inhibition induced ferroptosis in amoeboid cancer cells. Spheroid invasive growth was markedly suppressed by Erastin but restored upon GSH supplementation, highlighting the protective role of GSH against oxidative stress.

3. Glutathione (GSH) supplementation supported amoeboid cancer cell features decreasing Reactive Oxygen Species caused by SLC7A11 loss. SLC7A11 and GSH maintained redox homeostasis. Metastatic amoeboid cancer cells could not cope with oxidative stress when SLC7A11 was inhibited.

2. Inspecting melanoma biopsies, we found that SLC7A11 protein levels are higher in metastatic lesions vs. primary tumours but also increased at the invasive front. This supports SLC7A11 upregulation as an adaptive feature of aggressive melanoma cells.

🔬 Key findings from our work:

1. SLC7A11 levels are higher in cancer cells with higher Myosin II activity and located at the invasive front of melanomas. SLC7A11 depletion in these cells reduced Myosin II activity and 3D invasion, highlighting its potential role in melanoma dissemination.

The results, published in @cp-cellreports.bsky.social could lead to new tests to spot the most aggressive cancers, and treatments to stop them spreading.

“If we take away the melanoma cells’ shield and armour, we could stop cancer in its tracks.’
- Lead researcher Prof @vickysanzmoreno.bsky.social