Qué mejor forma de empezar a celebrar el #11F q acompañada por Ana María Rocha, radióloga de la Unidad de Mama del H. Álvaro Cunqueiro, en el Colegio Rosalía de Castro, rodeadas de mentes curiosas y futuras científicas 💜🔬👩‍🔬

#Conócelas @aseica.bsky.social @cinbio.bsky.social @uvigo.bsky.social

‼️ 🚀 We are hiring: #Postdoctoral Researcher

#SomosCIGUS #teamCINBIO #ignicia #gain @Xunta @galiciacrece @cinbio.bsky.social @uvigo.bsky.social

A few days before finishing this year, I want to thank all the wonderful people who surrounded and supported us during 2025 💙 It was a great year, full of new results, projects, recognitions, and collaborations. Thanks to all of you, More to come in 2026!🚀👩‍🔬🧑‍🔬 @cinbio.bsky.social @uvigo.bsky.social

www.farodevigo.es/gran-vigo/20... @cinbio.bsky.social @uvigo.bsky.social

Mural #MulleresNaCiencia de Expostas en #Vigo con @msmelanoma.bsky.social

Mujeres brillantes, valientes, resilentes, líderes e inspiradoras 💜

🧠 We show for the first time that (1) Cx43–lamin interaction alters DNA repair pathway choice, boosting therapy, preventing resistance, and resensitizing resistant tumours, and (2) we have developed a smart strategy to deliver Cx43 mRNA to tumours🚀

This is our model👇

💊 Restoring Cx43 in tumour cells has been challenging.
After testing multiple strategies, extracellular vesicles (EVs) proved most effective, delivering both Cx43 protein (via their membranes) and Cx43 mRNA, by engineering the EV-producing cells

🎯 Most importantly, restoring Cx43 avoided drug resistance in vitro and prevented resistance in vivo.
Even better, drug-resistant cells, which are more vulnerable to DNA damage, became more sensitive to Cx43 restoration 💪

🧬Thanks to @Gsabiolab @DNA_Repair_USC & @PabloHuertasLab we found that this interaction recruits DNA damage foci to the nuclear membrane, restricting HR & promoting error-prone repair driving genomic instability, which is further enhanced by DNA-damaging drugs like BRAF/MEKi💥

🔍 What did we find? Surprisingly, Cx43 antitumour effects in BRAF- (and NRAS)-mutant tumours do not seem to rely on its channel activity. Instead, we found Cx43 localizes to the nucleus and strongly interacts with nuclear lamin and DNA repair proteins⚙️

💭Cx43 shows antitumour activity in many cancers, but the mechanism remained controversial. We hypothesized that restoring Cx43 could help the microenvironment suppress growth and boost therapy response via its channel activity; a “kiss of death”

💥Check out our latest work in @NatureComms We identify a new target to impair DNA repair🧬inducing #senescence and #celldeath through synthetic lethality in combination with cancer therapy🧵

🔗Open access PDF: rdcu.be/euQkW

Today is the last day of Jolita and Tomas from @IMCentras in the lab!

It has been a pleasure to host them these last weeks through @Everest_MSCA
They will still join the CINBIO Annual Meeting at @MuseoMARCO tomorrow. Great talks and speakers ahead! ✨