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Assembling Molecular Shuttles Powered by Reversibly Attached Kinesins
Published on: January 26, 2019
Reprogramming ligand-receptor interactions via a self-powered molecular engine for proton-responsive regulation of
Yang Li1, Hui Wang1, Guofang Zhang2
1College of Chemistry and Chemical Engineering, Qingdao Key Laboratory of Intelligent Molecular Manufacturing and Precise Health, Shandong Provincial Key Laboratory of Intelligent Molecular Science and Engineering, Qingdao University, Qingdao, 266071, PR China.
Biosensors & Bioelectronics
|August 3, 2026
Summary
This study introduces an enzyme biofuel cell-based molecular engine to control cell movement by reprogramming ligand-receptor interactions. The system suppresses tumor cell migration by blocking the c-Met pathway.
Area of Science:
- Biomedical Engineering
- Molecular Biology
- Chemical Engineering
Background:
- Ligand-receptor interactions (LRIs) regulate cell motility and disease. Engineering molecular engines for LRIs is challenging due to low chemical cue density and scaffold limitations.
- Enzymatic biofuel cells (EBFCs) offer a solution by converting biofuels into energy for self-powered molecular tools, overcoming limitations of traditional chemical engines.
Purpose of the Study:
- To develop an enzyme biofuel cell-based self-powered molecular engine (EBFC-SME) for user-defined manipulation of LRIs and cell motility.
- To demonstrate the EBFC-SME's capability in reprogramming proton-responsive HGF/c-Met interactions for cancer therapy.
Main Methods:
- Constructed an EBFC-SME with a glucose dehydrogenase (GDH) bioanode and a bilirubin oxidase (BOD)/functional nucleic acids (FNAs)-coated biocathode.
- Utilized glucose-initiated redox reactions to generate protons and release FNAs for in-situ assembly on tumor cell membranes.
- Investigated the suppression of c-Met pathway activation and tumor cell migration.
Main Results:
- The EBFC-SME successfully generated protons and released FNAs, leading to the assembly on tumor cell membranes.
- Demonstrated the reprogramming of HGF/c-Met interactions, effectively blocking c-Met pathway activation.
- Significantly suppressed tumor cell migration, showcasing the engine's potential in cancer therapy.
Conclusions:
- The EBFC-SME platform provides a novel "sensing-conversion-initiation" tool for chemical regulation of cellular motility.
- This approach offers efficient regeneration of chemical cues via intrinsic energy conversion, enabling precise manipulation of LRIs.
- The EBFC-SME holds significant promise for applications in precision biomedicine and cancer treatment.
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