{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee JH"],"funding":["Pukyong National University"],"pagination":["533"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11677583"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(12)"],"pubmed_abstract":["Melanoma is an aggressive skin cancer with a high risk of cancer-related deaths, and inducing apoptosis in melanoma cells is a promising therapeutic strategy. This study investigates the anti-tumor potential of a novel lucknolide derivative LA-UC as a therapeutic candidate for melanoma. Lucknolide A (LA), a tricyclic ketal-lactone metabolite isolated from marine-derived <i>Streptomyces</i> sp., was chemically modified by introducing a 10-undecenoyl group to synthesize LA-UC. LA-UC preferentially inhibited the proliferation of melanoma cells, including B16F10, while exerting minimal effects on normal melanocytes or other tumor cell types, indicating the selective action of LA-UC against melanoma cells. LA-UC decreased G2/M checkpoint proteins, including cyclin B1 and Cdc2, while activating "],"journal":["Marine drugs"],"pubmed_title":["A Lucknolide Derivative Induces Mitochondrial ROS-Mediated G2/M Arrest and Apoptotic Cell Death in B16F10 Mouse Melanoma Cells."],"pmcid":["PMC11677583"],"funding_grant_id":["2023"],"pubmed_authors":["Park SJ","Kim M","Lee JH","Choi BK","Shin HJ"],"additional_accession":[]},"is_claimable":false,"name":"A Lucknolide Derivative Induces Mitochondrial ROS-Mediated G2/M Arrest and Apoptotic Cell Death in B16F10 Mouse Melanoma Cells.","description":"Melanoma is an aggressive skin cancer with a high risk of cancer-related deaths, and inducing apoptosis in melanoma cells is a promising therapeutic strategy. This study investigates the anti-tumor potential of a novel lucknolide derivative LA-UC as a therapeutic candidate for melanoma. Lucknolide A (LA), a tricyclic ketal-lactone metabolite isolated from marine-derived <i>Streptomyces</i> sp., was chemically modified by introducing a 10-undecenoyl group to synthesize LA-UC. LA-UC preferentially inhibited the proliferation of melanoma cells, including B16F10, while exerting minimal effects on normal melanocytes or other tumor cell types, indicating the selective action of LA-UC against melanoma cells. LA-UC decreased G2/M checkpoint proteins, including cyclin B1 and Cdc2, while activating ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2025-04-04T02:22:45.739Z","creation":"2025-04-04T02:22:45.739Z"},"accession":"S-EPMC11677583","cross_references":{"pubmed":["39728108"],"doi":["10.3390/md22120533"]}}