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Updated: Sep 12, 2025

11:32
Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
Published on: March 27, 2020
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CD133 + Vesicles Mediate Resistance to RAS-ERK Inhibition Regulated by YAP Activation in Liver Cancer Cells
Biorxiv : the Preprint Server for Biology
|August 6, 2025
Summary
CD133 protein forms vesicles that help cancer cells survive stress by communicating. This process is regulated by the Hippo-YAP pathway, offering new targets for liver cancer treatment.
Area of Science:
- Cell Biology
- Cancer Research
- Molecular Biology
Background:
- CD133 is a plasma membrane protein known as a stem cell biomarker.
- CD133+ intracellular vesicles (intercellsomes) mediate cell-cell communication under stress.
- The regulation and significance of CD133+ vesicles remain largely unknown.
Purpose of the Study:
- To investigate the role of CD133+ vesicles in cancer cell stress response.
- To elucidate the regulatory mechanism of CD133+ vesicle formation.
- To explore the therapeutic potential of targeting CD133 in liver cancer.
Main Methods:
- Inducing proliferative stress using MEK inhibitors in cancer cells.
- Analyzing CD133 expression and vesicle formation.
- Investigating the Hippo-YAP signaling pathway's role.
- Evaluating CD133's function in a mouse model of liver cancer.
Main Results:
- CD133 expression and vesicle formation are induced by MEK inhibitor-mediated stress.
- CD133+ vesicles are crucial for maintaining cancer cell proliferation under stress.
- MEK inhibition activates the Hippo-YAP pathway, promoting CD133 transcription and vesicle biogenesis.
- CD133 is critical for YAP-driven liver cancer progression in mice.
Conclusions:
- CD133 acts as a stress response marker in cancer cells, with its vesicles facilitating proliferation.
- The Hippo-YAP pathway regulates CD133+ vesicle biogenesis, linking YAP signaling to stress adaptation.
- CD133+ vesicles play a significant role in liver cancer progression and suggest therapeutic strategies for relapse.
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