Lobaric Acid Exhibits Anticancer Potential by Modulating the Wnt/β-Catenin Signaling Pathway in MCF-7 Cells
Özet
Lichen secondary metabolites with many remarkable biological activities are used in cancer treatments due to their low side effects and high anticancer potential. In particular, these metabolites constitute an interesting research area in cancer treatments due to their potential to induce apoptosis and suppress metastasis by inhibiting cancer-related signaling pathways. The Wnt/β-catenin signaling pathway plays a role in important biological processes such as oncogenesis, cell cycle regulation, cell proliferation, metastasis, differentiation, apoptosis, and drug resistance. Therefore, inhibition of this pathway is a potential target in cancer therapies. There is no detailed study explaining the potential anticancer molecular mechanism of the lichen secondary metabolite lobaric acid (LA) on breast cancer. Here, it is aimed to investigate the effect of LA on viability, apoptosis, and migration in MCF-7 cells and to elucidate the relationship between the potential anticancer effect and the Wnt/β-catenin signaling pathway. The dose- and time-dependent viability of LA-treated MCF-7 cells was evaluated by XTT assay, and the IC50 value was determined as 44.21 μg/mL at 48 h. LA increased the apoptotic cell population, as shown by flow cytometry analysis, qPCR, and Western blot results. LA inhibited β-catenin by inducing GSK3-β protein expression, thereby suppressing Wnt/β-catenin target genes. LA might be a natural active compound candidate for breast cancer treatment. © 2025 The Author(s). Pharmacology Research & Perspectives published by British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics and John Wiley & Sons Ltd.
Anahtar Kelimeler
Tam Kayıt
| Alan | Değer | Dil |
|---|---|---|
| dc.contributor.author | Kalın, Şeyda Nur | |
| dc.contributor.author | Bayındırlı, Kübra Nur | |
| dc.contributor.author | Toraman, Emine | |
| dc.contributor.author | Günaydın, Şükran | |
| dc.contributor.author | Keleş, Fatmanur | |
| dc.contributor.author | Altay, Ahmet | |
| dc.contributor.author | Budak, Harun | |
| dc.date.accessioned | 2026-10-18T20:25:55.792471909Z | |
| dc.date.available | 2026-10-18T20:25:55.792471909Z | |
| dc.date.issued | 2025 | |
| dc.description.abstract | Lichen secondary metabolites with many remarkable biological activities are used in cancer treatments due to their low side effects and high anticancer potential. In particular, these metabolites constitute an interesting research area in cancer treatments due to their potential to induce apoptosis and suppress metastasis by inhibiting cancer-related signaling pathways. The Wnt/β-catenin signaling pathway plays a role in important biological processes such as oncogenesis, cell cycle regulation, cell proliferation, metastasis, differentiation, apoptosis, and drug resistance. Therefore, inhibition of this pathway is a potential target in cancer therapies. There is no detailed study explaining the potential anticancer molecular mechanism of the lichen secondary metabolite lobaric acid (LA) on breast cancer. Here, it is aimed to investigate the effect of LA on viability, apoptosis, and migration in MCF-7 cells and to elucidate the relationship between the potential anticancer effect and the Wnt/β-catenin signaling pathway. The dose- and time-dependent viability of LA-treated MCF-7 cells was evaluated by XTT assay, and the IC50 value was determined as 44.21 μg/mL at 48 h. LA increased the apoptotic cell population, as shown by flow cytometry analysis, qPCR, and Western blot results. LA inhibited β-catenin by inducing GSK3-β protein expression, thereby suppressing Wnt/β-catenin target genes. LA might be a natural active compound candidate for breast cancer treatment. © 2025 The Author(s). Pharmacology Research & Perspectives published by British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics and John Wiley & Sons Ltd. | |
| dc.description.sponsorship | Funding: Open access funding provided by the Scientific and Technological Research Council of T\u00FCrkiye (T\u00DCB\u0130TAK). The authors received no specific funding for this work. The authors have nothing to report. | |
| dc.identifier.doi | 10.1002/prp2.70142 | |
| dc.identifier.issn | 2052-1707 | |
| dc.identifier.issue | 4 | |
| dc.identifier.pmcid | PMC12203569 | |
| dc.identifier.pmid | 40576246 | |
| dc.identifier.scopus | 2-s2.0-105009325190 | |
| dc.identifier.startpage | e70142 | |
| dc.identifier.uri | https://rdlopen.rawdatalibrary.net/r/ebyu/10792 | |
| dc.identifier.volume | 13 | |
| dc.identifier.wos | WOS:001518159000001 | |
| dc.language.iso | en | |
| dc.publisher | John Wiley and Sons Inc | |
| dc.relation.ispartof | Pharmacology Research and Perspectives | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | apoptosis | |
| dc.subject | breast cancer | |
| dc.subject | cytotoxicity | |
| dc.subject | expression | |
| dc.subject | Wnt/β-catenin pathway | |
| dc.subject | Antineoplastic Agents | |
| dc.subject | beta Catenin | |
| dc.subject | Breast Neoplasms | |
| dc.subject | Cell Movement | |
| dc.subject | Cell Proliferation | |
| dc.subject | Cell Survival | |
| dc.subject | Female | |
| dc.subject | Glycogen Synthase Kinase 3 beta | |
| dc.subject | Humans | |
| dc.subject | Lichens | |
| dc.subject | MCF-7 Cells | |
| dc.subject | Wnt Signaling Pathway | |
| dc.subject | acid | |
| dc.subject | glycogen synthase kinase 3beta | |
| dc.subject | Lobaric Acid | |
| dc.subject | protein Bax | |
| dc.subject | protein bcl 2 | |
| dc.subject | protein p53 | |
| dc.subject | unclassified drug | |
| dc.subject | antineoplastic agent | |
| dc.subject | antineoplastic activity | |
| dc.subject | Article | |
| dc.subject | cancer growth | |
| dc.subject | carcinogenesis | |
| dc.subject | cell cycle | |
| dc.title | Lobaric Acid Exhibits Anticancer Potential by Modulating the Wnt/β-Catenin Signaling Pathway in MCF-7 Cells | |
| dc.type | Article | |
| dspace.entity.type | Publication | |
| rdl.citation.scopus | 3 | |
| rdl.citation.wos | 3 | |
| rdl.department | Department of Chemistry, Faculty of Science and Arts, Erzincan Binali Yıldırım University, Erzincan, Turkey. | |
| rdl.oa.status | gold | |
| rdl.source.index | SCOPUS | |
| rdl.source.index | WOS | |
| rdl.source.index | PUBMED | |
| rdl.wos.index | Science Citation Index Expanded (SCI-EXPANDED) |
