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Updated: Jul 16, 2026

Inducible LAP-tagged Stable Cell Lines for Investigating Protein Function, Spatiotemporal Localization and Protein Interaction Networks
Published on: December 24, 2016
LAPSER1 is a putative cytokinetic tumor suppressor that shows the same centrosome and midbody subcellular
1Department of Pharmacology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
Abstract:
Prostate cancer is one of the most common cancers in men, with more than 500,000 new worldwide cases reported annually, resulting in 200,000 deaths of mainly older men in developed countries. Existing treatments have not proved very effective in managing prostate cancer, and continuing efforts therefore are ongoing to explore novel targets and strategies for future therapies. LAPSER1 has been identified as a candidate tumor suppressor gene in prostate cancer, but its true functions remain unknown. We report here that LAPSER1 colocalizes to the centrosomes and midbodies in mitotic cells with gamma-tubulin, MKLP1, and p80 katanin, and is involved in cytokinesis. Moreover, RNAi-mediated disruption of LAPSER1, which is accompanied by the mislocalization of p80 katanin, results in malformation of the central spindle. Significantly, the enhanced expression of LAPSER1 induces binucleation and renders the cells resistant to oncogenic transformation. In cells transformed by the v-Fps oncogene, overexpressed LAPSER1 induces abortive cytokinesis, followed by mitotic catastrophe in a p80 katanin-dependent manner. Cells that are rescued from this apoptotic pathway with Z-VAD-fmk display karyokinesis. These results suggest that LAPSER1 participates in cytokinesis by interacting with p80 katanin, the disruption of which may potentially cause genetic instability and cancer.
Insights
LAPSER1, a potential tumor suppressor, is crucial for cell division in prostate cancer. Its disruption leads to abnormal cell structures and potential genetic instability, offering new therapeutic targets.
Area of Science:
- Oncology
- Cell Biology
- Molecular Genetics
Background:
- Prostate cancer is a leading cause of cancer death in men worldwide.
- Current treatments for prostate cancer have limited efficacy, necessitating the search for novel therapeutic strategies.
- The tumor suppressor role of LAPSER1 in prostate cancer is suspected but not fully understood.
Purpose of the Study:
- To elucidate the function of LAPSER1 in prostate cancer cells.
- To investigate the role of LAPSER1 in cell division and cytokinesis.
- To explore the potential of LAPSER1 as a therapeutic target for prostate cancer.
Main Methods:
- Immunofluorescence microscopy to determine LAPSER1 localization in mitotic cells.
- RNA interference (RNAi) to disrupt LAPSER1 expression.
- Analysis of cell morphology, binucleation, and mitotic catastrophe.
- Investigation of LAPSER1 interaction with p80 katanin.
Main Results:
- LAPSER1 localizes to centrosomes and midbodies, interacting with key proteins involved in cell division.
- Disruption of LAPSER1 leads to defects in the central spindle and cytokinesis, resulting in binucleation.
- Overexpression of LAPSER1 confers resistance to oncogenic transformation and induces mitotic catastrophe in a p80 katanin-dependent manner.
- LAPSER1's interaction with p80 katanin is essential for proper cytokinesis.
Conclusions:
- LAPSER1 plays a critical role in cytokinesis, likely through its interaction with p80 katanin.
- Disruption of LAPSER1 function can lead to genetic instability, a hallmark of cancer.
- LAPSER1 represents a promising novel target for prostate cancer therapy.
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