Kinesin 5B and Its Role in Cancer Cell Autophagy and Death
Author Information
Author(s): Cardoso Carla M. P., Groth-Pedersen Line, Høyer-Hansen Maria, Kirkegaard Thomas, Corcelle Elizabeth, Andersen Jens S., Jäättelä Marja, Nylandsted Jesper
Primary Institution: Center for Neuroscience and Cell Biology, Faculty of Medicine, University of Coimbra, Portugal; Apoptosis Department and Centre for Genotoxic Stress Research, Institute of Cancer Biology, Danish Cancer Society, Copenhagen, Denmark; Centre for Experimental Bioinformatics (CEBI), University of Southern Denmark, Odense, Denmark
Hypothesis
KIF5B is a cancer-relevant lysosomal motor protein that affects lysosomal distribution and stability.
Conclusion
KIF5B is identified as a crucial motor protein for lysosomal function and autophagosome formation in cancer cells.
Supporting Evidence
- KIF5B was the only microtubule motor associated with lysosomes in MCF-7 cells.
- Depletion of KIF5B led to lysosomal destabilization and cell death in HeLa cells.
- KIF5B depletion inhibited the accumulation of autophagosomes in MCF-7 cells.
- KIF5B is highly expressed in various cancer cell lines.
- KIF5B depletion caused peripheral aggregations of lysosomes in HeLa cells.
- KIF5B is involved in the transport of components necessary for autophagosome formation.
Takeaway
KIF5B helps move important parts inside cancer cells, and when it's not working, the cells can die or have problems with cleaning up waste.
Methodology
Mass spectrometry was used to analyze lysosomal proteomes, and RNA interference was applied to deplete KIF5B in cancer cell lines.
Potential Biases
Potential bias in the interpretation of results due to reliance on specific cell lines.
Limitations
The study primarily focuses on two cancer cell lines, which may not represent all cancer types.
Participant Demographics
The study involved human breast carcinoma (MCF-7), cervix carcinoma (HeLa), and osteosarcoma (U2OS) cell lines.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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