Academic Journal
Microcolin A, a lipopeptide from marine cyanobacteria, suppresses the non-small cell lung carcinoma by regulating the C-terminal of Hsp90α and ROS/ERK signaling pathways.
| Τίτλος: | Microcolin A, a lipopeptide from marine cyanobacteria, suppresses the non-small cell lung carcinoma by regulating the C-terminal of Hsp90α and ROS/ERK signaling pathways. |
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| Συγγραφείς: | Lu Z; Experimental Training Center of Basic Medical Science, Naval Medical University, Shanghai 200433, China., Wang J; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China., Li S; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China., Jiang W; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China., Zhang X; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China., Ning Y; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China., Xu Y; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China., Jiao B; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China., Hu B; Naval Medical Center of PLA, Naval Medical University, Shanghai 200433, China., Yu H; Naval Medical Center of PLA, Naval Medical University, Shanghai 200433, China. Electronic address: yuhaobing@smmu.edu.cn., Lu X; Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai 200433, China. Electronic address: luxiaoling@smmu.edu.cn. |
| Πηγή: | Biochemical pharmacology [Biochem Pharmacol] 2026 Oct; Vol. 252, pp. 118195. Date of Electronic Publication: 2026 Jun 26. |
| Τύπος έκδοσης: | Journal Article |
| Γλώσσα: | English |
| Στοιχεία περιοδικού: | Publisher: Elsevier Science Country of Publication: England NLM ID: 0101032 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-2968 (Electronic) Linking ISSN: 00062952 NLM ISO Abbreviation: Biochem Pharmacol Subsets: MEDLINE |
| Imprint Name(s): | Publication: Oxford : Elsevier Science Original Publication: Oxford, New York [etc.] Paragamon Press. |
| Ιατρικοί όροι (MeSH): | Carcinoma, Non-Small-Cell Lung*/metabolism , Carcinoma, Non-Small-Cell Lung*/drug therapy , HSP90 Heat-Shock Proteins*/metabolism , HSP90 Heat-Shock Proteins*/antagonists & inhibitors , Reactive Oxygen Species*/metabolism , Lung Neoplasms*/drug therapy , Lung Neoplasms*/metabolism , MAP Kinase Signaling System*/drug effects , MAP Kinase Signaling System*/physiology , Lipopeptides*/pharmacology , Lipopeptides*/therapeutic use , Lipopeptides*/isolation & purification , Cyanobacteria*/chemistry, Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Xenograft Model Antitumor Assays/methods ; Apoptosis/drug effects ; Humans ; Animals ; Mice, Nude ; Cell Line, Tumor ; Mice ; Mice, Inbred BALB C ; Male |
| Περίληψη: | Lung cancer remains to be the leading cause of cancer-related mortality worldwide, with non-small cell lung carcinoma (NSCLC) accounting for approximately 85% and the five-year survival rate below 20%. Microcolin A (Mic A), a lipopeptide derived from marine cyanobacteria, exhibits significant antitumor activity, however, its underlying mechanism is unclear. Hsp90 is highly expressed in various cancer tissues and positively correlated with tumor progression and aggressiveness. Existing studies have shown that most Hsp90 inhibitors target the N-terminal ATP-binding pockets, however, the clinical trials of the relevant candidate drugs have been halted or postponed for insufficient stratification and side effects. In contrast, targeting the C-terminal domain of Hsp90 may be a more promising route to develop the anti-cancer drug. In this study, we find that Hsp90α is a potential target for Mic A, which could target the C-terminal of Hsp90α and suppress its expression in NSCLC cells. Mic A could also induce the apoptosis of NSCLC cells through reactive oxygen species (ROS) and ERK phosphorylation pathways, and the autophagy process may also be involved in the mechanism. In the NSCLC xenograft tumor model, Mic A could significantly reduce the growth of xenograft tumors by reducing Hsp90 and upregulating ERK phosphorylation. Overall, our research provides a broader perspective for a deeper understanding of the development of anti-tumor drugs targeting Hsp90, and the mechanism of intracellular downstream signaling pathways. And the Mic A, a tool molecule derived from the ocean, could provide significant references for the future development of anti-NSCLC. (Copyright © 2026. Published by Elsevier Inc.) |
| Competing Interests: | Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. |
| Contributed Indexing: | Keywords: Apoptosis; ERK phosphorylation; Hsp90α; Microcolin A; NSCLC; ROS |
| Substance Nomenclature: | 0 (HSP90 Heat-Shock Proteins) 0 (Reactive Oxygen Species) 0 (Lipopeptides) 0 (Antineoplastic Agents) |
| Entry Date(s): | Date Created: 20260626 Date Completed: 20260813 Latest Revision: 20260813 |
| Update Code: | 20260814 |
| DOI: | 10.1016/j.bcp.2026.118195 |
| PMID: | 42361915 |
| Βάση Δεδομένων: | MEDLINE |
| ISSN: | 1873-2968 |
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| DOI: | 10.1016/j.bcp.2026.118195 |