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| Autores principales: | , , , , , , , , , , |
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| Formato: | Artículo científico |
| Lenguaje: | en |
| Publicado: |
Scientific reports
2024
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| Materias: | |
| Acceso en línea: | https://pubmed.ncbi.nlm.nih.gov/39528552/ |
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- Elucidation of anti-human melanoma and anti-aging mechanisms of compounds from green seaweed Caulerpa racemosa. Wicaksono, Danar Taslim, Nurpudji Astuti Lau, Vincent Syahputra, Rony Abdi Alatas, Aiman Idrus Putra, Purnawan Pontana Tallei, Trina Ekawati Tjandrawinata, Raymond Rubianto Tsopmo, Apollinaire Kim, Bonglee Nurkolis, Fahrul Humans Endoplasmic Reticulum Chaperone BiP Melanoma Cell Line, Tumor Seaweed Endoribonucleases Animals Proto-Oncogene Proteins B-raf Mice TOR Serine-Threonine Kinases Protein Serine-Threonine Kinases Molecular Docking Simulation Sirtuin 1 Heat-Shock Proteins Aging Plant Extracts AMP-Activated Protein Kinases Human melanoma is linked with aging-related disorders, prompting interest in the development of functional foods derived from natural ingredients to mitigate its incidence. Molecules in green seaweeds such as Caulerpa racemosa can serve this purpose due to their anti-tumor and anti-inflammatory properties. A previous work study compounds profiling has been carried out, and in this research the molecular docking studies targeting receptors associated with melanoma (GRP78, IRE1, BRAF) and aging (mTOR, AMPK, SIRT1) identified four promising compound in an extract of C. racemosa. The current study aims to the mechanism of those compounds at a cellular level using the human A375 (BRAF-V600E mutation) and A375 and B16-F10 cell lines. The MTT assay was used to evaluate the potential of GSCRE compounds against A375 and B16-F10 cell lines, with comparisons made to normal HDFa cell lines. Results indicated that compound C2, also known as Caulersin, demonstrated a significantly different ∆G affinity binding score compared to the control drug Dabrafenib. GSCRE crude extract, particularly C2, showed potential in modulating mTOR, AMPK, and SIRT1 pathways and downregulating GRP78, IRE1, and BRAF signaling (p