Decreased Endothelin-1 bioavailability impairs aggressiveness of gallbladder cancer cells.

ABSTRACT:

Background

Gallbladder cancer (GBC) is a highly lethal malignancy, often diagnosed at advanced stages when curative options are limited. Its rapid progression and high metastatic potential result in a 5-year survival rate below 5%. Recent evidence highlights the role of Endothelin-1 (ET1), a bioactive peptide, in promoting tumor aggressiveness through activation of its receptors (ETRs). However, therapeutic strategies have mainly focused on receptor inhibition, neglecting the modulation of ET1 availability. Therefore, this study aimed to evaluate the therapeutic potential of modulating ET1 levels through the application of recombinant Neprilysin (rNEP) to degrade ET1 or inhibition of Endothelin Converting Enzyme-1 (ECE1) to reduce its production in GBC cells.

Methods

The eff

SUBMITTER: Vidal-Vidal J 

PROVIDER: S-EPMC12366186 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature