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Erschienen in: Clinical and Translational Oncology 8/2015

01.08.2015 | Research Article

CMTM3 is reduced in prostate cancer and inhibits migration, invasion and growth of LNCaP cells

verfasst von: F. Hu, W. Yuan, X. Wang, Z. Sheng, Y. Yuan, C. Qin, C. He, T. Xu

Erschienen in: Clinical and Translational Oncology | Ausgabe 8/2015

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Abstract

Purpose

A novel tumor suppressor gene CKLF-like MARVEL transmembrane domain-containing member 3 (CMTM3) is reduced or undetectable in many kinds of cancers and relates tumor malignant features. We detected its role in prostate cancer for possibility of target therapy as accumulating evidence has shown that CMTM3 is a promising tumor suppressor gene (TSG) for gene therapy.

Methods

The expression of CMTM3 detected in prostate tissue microarray, specimens and cell lines were evaluated by immunohistochemistry and semi-quantitative PCR and Western blot, respectively. After being transfected with CMTM3 adenovirus or vector (mock), the proliferation and migration and invasion of LNCaP cells were detected by transwell assay and matrigel assay, respectively. Furthermore, the effects of CMTM3 on tumor growth were performed in nude mice xenograft in vivo.

Results

We found CMTM3 was reduced in PCa tissues and cells compared with BPH tissues, and its expression in PCa tissues was related to the Gleason score. Moreover, after being transfected with adenovirus, ectopic expression of CMTM3 in LNCaP cells led to significant inhibition of cell proliferation and migration and invasion compared with the control (P < 0.05), which may be attributed to decreased Erk1/2 activity as p-Erk1/2 was remarkably reduced when CMTM3 was overexpressed. Finally, restoration of CMTM3 significantly suppressed xenograft tumor growth in vivo (P < 0.01).
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Metadaten
Titel
CMTM3 is reduced in prostate cancer and inhibits migration, invasion and growth of LNCaP cells
verfasst von
F. Hu
W. Yuan
X. Wang
Z. Sheng
Y. Yuan
C. Qin
C. He
T. Xu
Publikationsdatum
01.08.2015
Verlag
Springer Milan
Erschienen in
Clinical and Translational Oncology / Ausgabe 8/2015
Print ISSN: 1699-048X
Elektronische ISSN: 1699-3055
DOI
https://doi.org/10.1007/s12094-015-1288-9

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