Peanut hairy root culture extract suppresses migration and invasion of highly metastatic cholangiocarcinoma cells
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Creator Suchada Phimsen
Title Peanut hairy root culture extract suppresses migration and invasion of highly metastatic cholangiocarcinoma cells
Contributor Piyathida Wongkham, Donruetai Thalapphet, Warissara Wongkham, Apinun Limmongkon
Publisher The Pharmacological and Therapeutic Society of Thailand
Publication Year 2569
Journal Title Journal of Basic and Applied Pharmacology
Journal Vol. 6
Journal No. 2
Page no. O77-88
Keyword cholangiocarcinoma, peanut hairy root culture extract, prenylated stilbenoids, cell migration, cell invasion
URL Website https://li01.tci-thaijo.org/index.php/JBAP
Website title เว็บไซต์คลังข้อมูล
ISSN 2774-0854 (Online)
Abstract Cholangiocarcinoma (CCA) is a highly aggressive malignancy withpoor prognosis, partly because of late-stage diagnosis, therapeutic resistance, and metastatic progression.This study investigated the anticancer and anti-migratory, and anti-invasive effects of peanut hairy root culture crude extract (PCE), a source of prenylatedstilbenoidsincluding trans-arachidin-1andtrans-arachidin-3. The effectsof PCE on cell viability wereinitially screened inKKU-213B, A549, MCF-7, and KBcancer cells. PCE reduced cell viability in a concentration-dependent manner, with KKU-213Bcells showing the greatest sensitivity among the tested cell lines. The effects of PCE on cell viabilitywere subsequently evaluatedin a panel of CCA cell linescomprisingKKU-213A, KKU-213B, KKU-055, and the highly metastatic KKU-213AL5subline.KKU-213AL5 cellsexhibited the greatest sensitivity and were therefore selected for further investigation. At non-cytotoxic concentrations, PCE significantly suppressed KKU-213AL5 cell migration andinvasion, as determined by wound-healing and Matrigel-coated Transwell assays, respectively. Gelatin zymography showedthat PCE did not significantly alterMMP-2orMMP-9 activity. Collectively, these findings demonstrate that PCE inhibitsthe cell viability, migration, and invasion of highly metastatic CCA cells,supportingfurther investigation of its active constituentsand underlying molecular mechanism.
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