ArticleCell death discovery2025
HapA protease targets PAR-1/2 to modulate ERK signalling and reduce cancer cell viability.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Integrative transcriptomic and proteomic profiling reveals altered thymocyte development and microenvironment remodeling during natural thymic atrophy.Frontiers in cell and developmental biology · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Recent studies reveal that Vibrio cholerae secretes virulence factors impacting host cell viability, though their effects on cancer cells remain unclear. However, the bacterial components and mechanisms influencing cancer cells remain largely unknown. This study investigated the effects of V. cholerae mutants lacking secreted proteins on carcinoma cells. We identified the hemagglutinin zinc-metalloprotease HapA as the main factor reducing cancer cell viability. HapA cleaves protease-activated receptors 1 and 2 on epithelial cancer cells at unique sites, unlike human proteases. This cleavage triggers an early and transient activation of the kinases MEK and ERK. Transient MEK and ERK activation initiates caspase 7, leading to apoptosis and reduced viability in epithelial cancer cells. Our findings underscore the significance of human protease-activated receptors as targets for bacterial protease HapA. Furthermore, we demonstrate that selective cleavage of PAR-1/2 by HapA adjusts MEK-ERK signalling dynamics, suggesting potential new avenues for the development of novel anticancer therapies. Understanding how pathogens like V. cholerae interact with cancer cells sheds light on potential mechanisms underlying cancer progression and suggests new therapeutic targets for cancer treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.