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Transmembrane prostatic acid phosphatase (TMPAP) interacts with snapin and deficient mice develop prostate
Ileana B Quintero1, Annakaisa M Herrala, César L Araujo
1Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital Laboratory, Helsinki, Finland.
Plos One
|September 17, 2013
Summary
Prostate cancer mechanisms were explored using PAP-deficient mice. Transmembrane prostatic acid phosphatase (TMPAP) interacts with snapin, affecting vesicular traffic and potentially driving prostate adenocarcinoma development.
Area of Science:
- Molecular biology
- Cancer research
- Cellular biology
Background:
- Prostate carcinogenesis mechanisms are unclear.
- Prostatic acid phosphatase (PAP) is linked to prostate cancer but its role is debated.
- Two PAP isoforms exist: secretory (sPAP) and transmembrane (TMPAP).
Purpose of the Study:
- To elucidate the physiological function of TMPAP in the prostate.
- To investigate the molecular mechanisms of prostate carcinogenesis involving PAP.
Main Methods:
- Histological, ultra-structural, and genome-wide analyses of PAP-deficient mice (PAP(-/-)).
- Yeast two-hybrid assays to identify PAP-interacting proteins.
- Co-localization studies and in vivo FRET analyses in transfected LNCaP cells.
- Exosome isolation and analysis.
Main Results:
- PAP(-/-) mice developed slow-growing, non-metastatic prostate adenocarcinoma.
- TMPAP interacts with snapin, a protein involved in vesicular membrane fusion.
- Dysregulation of genes related to synaptic vesicular traffic was observed.
- Both TMPAP and snapin were found in isolated exosomes.
Conclusions:
- TMPAP is implicated in endo-/exocytosis processes.
- Disturbed vesicular traffic is a key feature of prostate adenocarcinoma.
- TMPAP's interaction with snapin may contribute to prostate carcinogenesis.
