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Updated: Mar 21, 2026

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
Published on: October 18, 2024
TMEPAI increases lysosome stability and promotes autophagy
Shenheng Luo1, Meng Yang1, Dan Lv1
1School of Biotechnology, Tianjin University of Science and Technology, Key Lab of Industrial Fermentation Microbiology of the Ministry of Education, Tianjin 300457, China.
Transmembrane prostate androgen-induced protein (TMEPAI) depletion destabilizes lysosomes and inhibits autophagy, increasing cancer cell sensitivity to chemotherapy. TMEPAI may be a therapeutic target for cancer treatment.
Area of Science:
- Cell Biology
- Cancer Research
- Molecular Biology
Background:
- Autophagy is crucial for cell metabolism and organelle maintenance in normal and cancer cells.
- Transmembrane prostate androgen-induced protein (TMEPAI) is a known pro-tumorigenic factor overexpressed in tumors.
Purpose of the Study:
- To investigate the role of TMEPAI in autophagy and lysosomal stability.
- To determine if TMEPAI influences cancer cell sensitivity to chemotherapy.
Main Methods:
- TMEPAI depletion in cancer cells.
- Assessment of lysosomal stability and autophagy markers.
- Evaluation of chemosensitivity.
Main Results:
- TMEPAI depletion caused lysosomal labilization and inhibited autophagy.
- Autophagy inhibition was linked to Beclin-1 regulation.
- Reduced TMEPAI enhanced cancer cell sensitivity to chemotherapeutic drugs.
Conclusions:
- TMEPAI promotes lysosome stability and autophagy.
- Targeting TMEPAI could enhance cancer chemotherapeutic efficacy.
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