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Inhibition of Plasminogen Activator Inhibitor-1 (PAI-1) by Tiplaxtinin Attenuates the Aggressive Phenotype of Vulvar Squamous Cell Carcinoma Cells In Vitro.

Created on 01 Jul 2026

Authors

Jaqueline Warmbold, Julia Gallwas, Carsten Gründker

Published in

In vivo (Athens, Greece). Volume 40. Issue 4. Pages 1915-1927.

Abstract

Vulvar squamous cell carcinoma (VSCC), while relatively rare, is associated with significant morbidity. Activation of G-protein coupled estrogen receptor 1 (GPER1), which has a tumor-suppressing effect in VSCC, leads to reduced expression of plasminogen activator inhibitor-1 (PAI-1). PAI-1, a key regulator of the plasminogen activation system, is overexpressed in various cancers and is linked to poor prognosis. Its role and potential as a therapeutic target in VSCC remain poorly explored. This study investigated the effects of the specific PAI-1 inhibitor tiplaxtinin (PAI-039, TPX) on the aggressive behavior of VSCC cells in vitro.
Expression of PAI-1 was verified by western blot. The effects of TPX treatment on viability, proliferation, migration, and invasion of A431 and Cal-39 VSCC cells were assessed using AlamarBlue, crystal violet, gap closure, and Boyden chamber assays, respectively. Apoptosis was examined using the Annexin V/propidium iodide (PI) assay.
Both VSCC cell lines showed PAI-1 expression. With increasing TPX concentrations, viability and proliferation of the VSCC cells decreased significantly. Cell migration and invasion were both significantly reduced under treatment with the PAI-1 inhibitor. Apoptosis was not significantly induced by TPX.
PAI-1 inhibitor TPX showed a strong inhibitory effect on VSCC cells, significantly reducing their viability, proliferation, migration and invasive capacity. This compound showed a strong ability to suppress important cell functions associated with cancer progression, making it a promising candidate for VSCC therapy to specifically inhibit growth and spread of VSCC.

PMID:
42379802
Bibliographic data and abstract were imported from PubMed on 01 Jul 2026.

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