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Orientational Transition in a Liquid Crystal Triggered by the Thermodynamic Growth of Interfacial Wetting Sheets
Published on: May 15, 2017
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Invasiveness-triggered state transition in malignant melanoma cells
Huan Wang1,2, Yan-Guo Zhang2, Jing Ma3
1Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi'an, China.
Journal of Cellular Physiology
|November 28, 2018
Summary
Melanoma cells can switch between epithelial and mesenchymal states, driven by invasion. Targeting the M3 muscarinic acetylcholine receptor (mAChR) may offer new strategies against malignant melanoma.
Area of Science:
- Oncology
- Cell Biology
- Dermatology
Background:
- Human melanoma exhibits significant cancer cell morphological heterogeneity.
- Epithelial cancer cells are prevalent across various human melanoma developmental stages.
Purpose of the Study:
- To investigate the mechanisms maintaining melanoma cells in an epithelial state.
- To explore the role of invasiveness in melanoma cell state transitions.
Main Methods:
- Utilized A2058 melanoma cell line for mechanistic studies.
- Employed transwell invasion assays and scratch assays to observe morphological changes.
- Analyzed epithelial-mesenchymal transition (EMT) markers (E-cadherin, vimentin) via immunofluorescence and co-immunoprecipitation.
- Investigated the M3 muscarinic acetylcholine receptor (mAChR) and p75 neurotrophin receptor (p75NTR) interaction.
- Used small interfering RNA (siRNA) to knockdown M3 mAChR expression.
Main Results:
- Transwell invasion, not scratch migration, induced morphological changes between epithelial and mesenchymal melanoma cells within 4 days.
- Morphological switch correlated with dynamic alterations in E-cadherin and vimentin.
- Observed uncoupling of M3 mAChR and p75NTR in epithelial melanoma cells.
- M3 mAChR knockdown inhibited the transition from mesenchymal to epithelial cell morphology.
Conclusions:
- Established a cellular model of invasiveness-triggered state transition (ITST) in melanoma.
- ITST provides a biological basis for maintaining metastatic melanoma cells in the epithelial state.
- M3 mAChR-mediated ITST presents a potential therapeutic target for inhibiting malignant melanoma progression.
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