Transmembrane prostatic acid phosphatase (TMPAP) delays cells in G1 phase of the cell cycle
CL Araujo, IB Quintero, K Ovaska, AM Herrala… - The …, 2016 - Wiley Online Library
CL Araujo, IB Quintero, K Ovaska, AM Herrala, S Hautaniemi, PT Vihko
The Prostate, 2016•Wiley Online LibraryBACKGROUND Prostate adenocarcinoma is the most common form of prostate cancer. We
have previously shown in a murine model that prostatic acid phosphatase (PAP) deficiency
leads to increased cell proliferation and development of prostate adenocarcinoma. The
association between PAP and prostate cancer has been reported. Indeed, high PAP
enzymatic activity is detected in the serum of patients with metastatic disease while its
expression is reduced in prostate cancer tissue. However, the molecular mechanisms …
have previously shown in a murine model that prostatic acid phosphatase (PAP) deficiency
leads to increased cell proliferation and development of prostate adenocarcinoma. The
association between PAP and prostate cancer has been reported. Indeed, high PAP
enzymatic activity is detected in the serum of patients with metastatic disease while its
expression is reduced in prostate cancer tissue. However, the molecular mechanisms …
BACKGROUND
Prostate adenocarcinoma is the most common form of prostate cancer. We have previously shown in a murine model that prostatic acid phosphatase (PAP) deficiency leads to increased cell proliferation and development of prostate adenocarcinoma. The association between PAP and prostate cancer has been reported. Indeed, high PAP enzymatic activity is detected in the serum of patients with metastatic disease while its expression is reduced in prostate cancer tissue. However, the molecular mechanisms behind the onset of the disease remains poorly understood. We previously identified a novel transmembrane prostatic acid phosphatase (TMPAP) isoform, which interacts with snapin. TMPAP is expressed on the plasma membrane, as well as endosomal/lysosomal and exosomal membrane vesicles by means of a tyrosine‐based lysosomal targeting motif (Yxxϕ).
METHODS
We used stable overexpression of the secreted isoform (SPAP) and TMPAP in LNCaP cells, live cell imaging, microarray and qRT‐PCR analyses, and fluid phase uptake of HRP and transferrin.
RESULTS
Our results indicate that the stable overexpression of TMPAP, but not SPAP in LNCaP cells reduces cell growth while increasing endo/exocytosis and cell size. Specifically, cells overexpressing TMPAP accumulate in the G1 phase of the cell cycle, and show altered gene expression profile.
CONCLUSIONS
Our data suggests that TMPAP may function as a non‐canonical tumor suppressor by delaying cell growth in G1 phase of the cell cycle. Prostate 76:151–162, 2016. © 2015 Wiley Periodicals, Inc.
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