Anticancer Effect of Pinostrobin on Human Breast Cancer Cells Through Regulation of Epithelial Mesenchymal Transition
17
Issued Date
2025-01-01
Resource Type
ISSN
15347354
eISSN
1552695X
Scopus ID
2-s2.0-105005449455
Journal Title
Integrative Cancer Therapies
Volume
24
Rights Holder(s)
SCOPUS
Bibliographic Citation
Integrative Cancer Therapies Vol.24 (2025)
Suggested Citation
Jongjang P., Likitnukul S., Reabroi S., Mangmool S., Nutho B., Pinthong D. Anticancer Effect of Pinostrobin on Human Breast Cancer Cells Through Regulation of Epithelial Mesenchymal Transition. Integrative Cancer Therapies Vol.24 (2025). doi:10.1177/15347354251341438 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/110379
Title
Anticancer Effect of Pinostrobin on Human Breast Cancer Cells Through Regulation of Epithelial Mesenchymal Transition
Author's Affiliation
Corresponding Author(s)
Other Contributor(s)
Abstract
Triple-negative breast cancer (TNBC) is the most aggressive type of breast cancer, with a high incidence of metastasis and chemoresistance. Epithelial-mesenchymal transition (EMT) is one of the molecular mechanisms that has been linked to the promotion of metastasis, and it can be promoted by several activators including the NF-κB signaling pathway. As a result, targeting EMT may be a potential strategy for treating TNBC. Pinostrobin is one of the important flavonoids found in the rhizome and rootlet of Boesenbergia rotunda (L.) Mansf. (fingerroot) that exhibits anticancer activities. However, the precise mechanism underlying the anticancer effect of pinostrobin on breast cancer remains unclear, and additional evidence is needed. In this study, the MCF-7 and MDA-MB-231 breast cancer cells were treated with various concentrations of pinostrobin. To determine the effect of pinostrobin on cell viability, an MTT assay was performed. Wound healing and Transwell chamber assays were conducted to examine the effect of pinostrobin on migration ability. RT-PCR was used to detect the expression of mRNA involved in NF-κB and EMT signaling pathways. The results revealed that low concentrations of pinostrobin did not affect cell viability, while higher concentrations produced an inhibitory effect on the viability of both cell lines. Pinostrobin also impeded migration and suppressed the expression of N-cadherin, a mesenchymal marker. Molecular docking analysis also suggested that the pinostrobin may target N-cadherin with higher binding affinity than IKK complex and NF-κB p65. These findings indicate that pinostrobin may serve as a potential treatment for TNBC.