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Biology subjects

Lozano, M. L.

Publications and source records attributed to Lozano, M. L..

2 recordsLinked to original sources

Analysis of AlphaFold and molecular dynamics structure predictions of mutations in serpins

Serine protease inhibitors (serpins) include thousands of structurally conserved proteins playing key roles in many organisms. Mutations affecting serpins may disturb their conformation, leading to inactive forms. Unfortunately, conformational consequences of mutations affecting serpins are difficult to predict. In this study we integrate experimental data of patients with mutations affecting one serpin with the predictions obtained by AlphaFold and molecular dynamics. Five SERPINC1 mutations causing antithrombin deficiency, the strongest congenital thrombophilia, (p.Arg79Cys; p.Pro112Ser, p.Met283Val; p.Pro352insValPheLeuPro, and p.Glu241_Leu242delinsValLeuValLeuValAsnThrArgThr-Ser) were selected from a cohort of 350 unrelated patients based on functional, biochemical, and crystallographic evidence supporting a folding defect. AlphaFold gave an accurate prediction for the wild-type antithrombin structure. However, it only produced native structures for all variants, regardless of its complexity and in-vivo conformational consequences. Similarly, molecular dynamics of up to 1000 ns at temperatures that caused conformational transitions did not show significant changes in the native structure of wild-type or variants. In conclusion, one predictive tool of protein folding, AlphaFold, and a simulation method for analyzing the physical movements of atoms and molecules, molecular dynamics, force predictions into the native stressed conformation at conditions with experimental evidence supporting a conformational change to relaxed structures. It is necessary to improve predictive strategies for serpins that consider the conformational sensitivity of these molecules.

bioinformatics↗

Pro-tumor and prothrombotic activities of hepsin in colorectal cancer cells and suppression by venetoclax

Hepsin is a type II transmembrane serine protease whose expression has been linked to greater tumorigenicity and worse prognosis in different tumors such as prostate and gastric cancer. Recently, our group described hepsin expression in the primary biopsy as a potential biomarker of thrombosis and metastasis in localized colorectal cancer patients. Here we explored the role of hepsin in this tumor. Hepsin overexpression increased Caco-2 cell migration and invasion, higher phosphorylation of Erk1/2 and STAT3 and led to more thrombin generation in plasma. Indeed, our study revealed higher plasma levels of hepsin in metastatic colorectal cancer patients, which was associated with a greater tendency toward thrombosis. By virtual screening of a FDA-approved drug library, we identified venetoclax as a potent hepsin inhibitor, reducing the metastatic and prothrombotic phenotype of Caco-2 cells, but not of other colorectal cancer cells without hepsin expression. Interestingly, pre-treating Caco-2 cells overexpressing hepsin with venetoclax reduced its in vivo invasiveness. Taken together, our results demonstrate that elevated hepsin levels correlate with a more aggressive and prothrombotic tumor phenotype. Likewise, they evidence an antitumor role for venetoclax as a hepsin inhibitor. This lays the groundwork for molecular targeted therapy for colorectal cancer.

cancer biology↗