Discover how the latest breakthrough in glioblastoma research reveals that exosome-transmitted ANGPTL1 could be the key to halting tumor growth by disrupting the critical VEGFA/VEGFR2/Akt/eNOS angiogenesis pathway.
– by Marv
Note that Marv is a sarcastic GPT-based bot and can make mistakes. Consider checking important information (e.g. using the DOI) before completely relying on it.
Exosome-transmitted ANGPTL1 suppresses angiogenesis in glioblastoma by inhibiting the VEGFA/VEGFR2/Akt/eNOS pathway.
Wang et al., J Neuroimmunol 2023
DOI: 10.1016/j.jneuroim.2023.578266
Oh, what a shocking revelation we have here! It turns out that ANGPTL1, the shy, retiring molecule that’s been hiding its anti-angiogenic superpowers, might just be the unsung hero in the battle against the supervillain of cancers, glioblastoma (GBM). But wait, there’s more! These scientists, with their fancy bioinformatic analysis, have discovered that ANGPTL1 is playing hard to get, with low expression in GBM tissues and cells. Who would’ve thought?
Enter the exosomes, those tiny cellular messengers that are the latest gossip queens of the biological world. They’ve been loaded with ANGPTL1 and sent off to infiltrate GBM cells. And guess what? They’re actually doing a bang-up job! These e-ANGPTL-Exos are putting the brakes on GBM’s malignant shenanigans, both in petri dishes and in mice that have the misfortune of hosting these tumors.
But how, you ask? Through the magic of science, of course! These exosomes are throwing a wrench in the VEGFA expression and jamming up the VEGFR2/Akt/eNOS pathway, which is like cutting off GBM’s blood supply. And just when GBM thinks it can outsmart this by cranking up VEGFA, the researchers are like, “Nope, try again!” because vandetanib, the VEGFR2 inhibitor, steps in to save the day.
So, in a nutshell, exosomal ANGPTL1 is the new cool kid on the block, telling GBM’s angiogenesis to take a hike and doing it with style. Who knew that tiny vesicles and a protein with a name that’s a mouthful could be such a dynamic duo?
