Nature CommunicationsBiochemistryPeer-reviewed journal article
Cycling Molecular Assemblies for Selective Cancer Cell Golgi Disruption
Weiyi TaniD, Qiuxin ZhangiD, Zhiyu Liu, Kangqiang QiuiD, Divyanshu MahajaniD, Thomas J. GertoniD, Noah CoppermaniD, Erica C. DresselhausiD, Chaoshuang XiaiD, Cheng Lin, William Lau, Mikki Lee, Isabela Ashton-Rickardt, Pengyu HongiD, Daniela M. DinulescuiD, Jer-Tsong HsiehiD, Avital Adah RodaliD, David Mark LoebiD, Ronny DrapkiniD, Jiajie DiaoiD, Lei LüiD, Bing XuiD
Abstract
The Golgi apparatus is a critical organelle responsible for intracellular trafficking and signaling, orchestrating essential processes such as protein and lipid sorting1-5. Dysregulation of its function has been implicated in various pathologies, including obesity, diabetes, and cancer, highlighting its importance as a potential therapeutic target. Despite this, the development of tools to selectively target the Golgi in specific cell types remain a significant unmet challenge in imaging and drug discovery. Golgi-specific enzyme activities, such as those mediated by protein acyltransferases and thioesterases6, offer an untapped opportunity to develop subcellularly localized therapeutics. Current approaches predominantly rely on direct protein binding but lack the necessary cell selectivity7, underscoring the unmet need for innovative strategies to selectively disrupt Golgi function in cancer cells. Here, we report the development of cycling molecular assemblies (CyMA), a novel class of small peptide derivatives (e.g., dipeptides), which exploit the unique enzymatic environment of the Golgi to establish futile cycles of reversible S-acylation. These assemblies selectively accumulate in cancer cell Golgi, interfering with protein S-acylation cycles and disrupting organelle homeostasis. CyMA impair key Golgi functions, including protein trafficking, glycosylation, and secretion, while demonstrating selective sparing hepatocytes and immune cells such as M1 macrophages. This selective activity represents a paradigm shift, utilizing an enzyme switch and leveraging intracellular environment rather than direct protein binding. Unlike conventional approaches, CyMA reduce tumor growth, drug resistance, and metastasis by pleiotropically disrupting Golgi related functions. By demonstrating the potential of futile cycles as a therapeutic strategy8, this study introduces a generalizable method for targeting organelle-specific enzyme activities. These findings not only underscore the therapeutic potential of CyMA in cancer but also pave the way for future applications in other Golgi-associated diseases.
- organism: human
- research focus: drug response / drug discovery
- research focus: cancer & tumor microenvironment
- research focus: cell type annotation
- research focus: cell signaling & trafficking
- approach: experimental assay
- Citations
- 6
- FWCI
- 4.48
- Field percentile
- top 7%
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