Dr. María D. Mayán
@mariamayan.bsky.social
Aging & Cancer. Connexins | Research Group Leader at @cinbio_uvigo | PI Horizon Europe consortiums | @uvigo | Committed to Women in Science and Equity
Mural #MulleresNaCiencia de Expostas en #Vigo con @msmelanoma.bsky.social
Mujeres brillantes, valientes, resilentes, líderes e inspiradoras 💜
Mujeres brillantes, valientes, resilentes, líderes e inspiradoras 💜
September 27, 2025 at 4:46 PM
Mural #MulleresNaCiencia de Expostas en #Vigo con @msmelanoma.bsky.social
Mujeres brillantes, valientes, resilentes, líderes e inspiradoras 💜
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👇
This is our model👇
July 28, 2025 at 7:54 PM
🧠 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👇
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
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
July 28, 2025 at 7:54 PM
💊 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
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 💪
Even better, drug-resistant cells, which are more vulnerable to DNA damage, became more sensitive to Cx43 restoration 💪
July 28, 2025 at 7:54 PM
🎯 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 💪
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💥
July 28, 2025 at 7:54 PM
🧬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⚙️
July 28, 2025 at 7:54 PM
🔍 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”
July 28, 2025 at 7:54 PM
💭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
🔗Open access PDF: rdcu.be/euQkW
July 28, 2025 at 7:54 PM
💥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
🔗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! ✨
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! ✨
July 9, 2025 at 8:01 PM
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! ✨
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! ✨