In vitro inhibition of migration and adhesionin cholangiocarcinoma cells by ovalitenin Athrough PI3K modulation
รหัสดีโอไอ
Creator Auemduan Prawan
Title In vitro inhibition of migration and adhesionin cholangiocarcinoma cells by ovalitenin Athrough PI3K modulation
Contributor Putu Ririn Andreani, Laddawan Senggunprai, Sarinya Kongpetch, Piman Pocasap, Chavi Yenjai, Arthan Supakorn
Publisher The Pharmacological and Therapeutic Society of Thailand
Publication Year 2569
Journal Title Journal of Basic and Applied Pharmacology
Journal Vol. 6
Journal No. 1
Page no. O1-12
Keyword Ovalitenin A, Millettia brandisiana, bile duct cancer, metastasis, PI3K signaling
URL Website https://li01.tci-thaijo.org/index.php/JBAP
Website title เว็บไซต์คลังข้อมูล
ISSN 2774-0854 (Online)
Abstract Ovalitenin A, a chalcone extractedfromthe roots of Millettia brandisianaKurz, has exhibitedcytotoxic propertiesinvarioushuman cancer cells. However, the effects of thison cholangiocarcinoma (CCA), an aggressive malignancy of the bile duct epithelium, are still not well understood. This study investigatedthe anti-metastatic potential of ovalitenin A and itsassociated molecular mechanismsin CCA cells. Sulforhodamine B (SRB), wound-healing, and adhesion assays were used to test cell viability, migration, and adhesion, respectively. Western blotting was performedto quantifyphosphorylated PI3K and VEGF proteins, andqRT-PCR was used to measureMMP-9and TIMP-1mRNA.Ovalitenin A suppressedthe proliferationof CCA cellsin a concentration-dependent manner. Following24 hours of treatment, it markedly diminishedcell migration and adhesion. Network pharmacologyanalysisfound 32 commontargetsbetween ovalitenin A and CCAutilizing the SwissTargetPrediction and GeneCards databases. Moreover, protein–protein interaction analysis revealed a robust associationamongthese targets, indicating the involvement of PI3K-related signaling pathways. PIK3CA and MMP-family proteins were prioritized as candidate targets based on their centrality within the network and their well-established roles in CCA progression, metastasis, and extracellular matrix remodeling. As predicted, treatment of ovalitenin A reduced the levels of phosphorylated PI3K and VEGF proteins and loweredthe ratio ofMMP-9to TIMP-1mRNA.These findings suggestthat ovalitenin A mayreduce CCA metastasis, possibly by altering PI3K signaling and its downstream molecular effectors.
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