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Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma

BACKGROUND: Pim-1 (Provirus integration site for Moloney murine leukemia virus 1) belongs to the Ser/Thr kinase family and plays a pivotal role in occurrence and development of oncogenesis. Recent studies have demonstrated that Pim-1 phosphorylates RUNX3 and alters its subcellular localization. Howe...

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Autores principales: Zhu, Xin, Xu, Jia-jie, Hu, Si-si, Feng, Jian-guo, Jiang, Lie-hao, Hou, Xiu-xiu, Cao, Jun, Han, Jing, Ling, Zhi-qiang, Ge, Ming-hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304190/
https://www.ncbi.nlm.nih.gov/pubmed/25551195
http://dx.doi.org/10.1186/s13046-014-0114-5
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author Zhu, Xin
Xu, Jia-jie
Hu, Si-si
Feng, Jian-guo
Jiang, Lie-hao
Hou, Xiu-xiu
Cao, Jun
Han, Jing
Ling, Zhi-qiang
Ge, Ming-hua
author_facet Zhu, Xin
Xu, Jia-jie
Hu, Si-si
Feng, Jian-guo
Jiang, Lie-hao
Hou, Xiu-xiu
Cao, Jun
Han, Jing
Ling, Zhi-qiang
Ge, Ming-hua
author_sort Zhu, Xin
collection PubMed
description BACKGROUND: Pim-1 (Provirus integration site for Moloney murine leukemia virus 1) belongs to the Ser/Thr kinase family and plays a pivotal role in occurrence and development of oncogenesis. Recent studies have demonstrated that Pim-1 phosphorylates RUNX3 and alters its subcellular localization. However, few studies have concerned the implications of Pim-1 in the salivary gland adenoid cystic carcinoma (ACC). In this study, we aimed to clarify the function of Pim-1 in ACC in vitro. Meanwhile, we measured the levels of Pim-1 and RUNX3 in the ACC tissues. The correlations between Pim-1/RUNX3 levels and clinical parameters were also analyzed. METHODS: SACC-83 and SACC-LM cells were transfected with the Pim-1 siRNA. Pim-1 mRNA and protein expression were measured using real-time PCR and immnuoblot, respectively. Cell proliferation was analyzed by CCK-8 assay. Cell cycle, apoptosis, and mitochondrial membrane potential were detected by flow cytometry. Effects of Pim-1 on cells’ invasion were evaluated by transwell migration assay. Pim-1 and RUNX3 levels in ACC tissues were examined by immunohistochemistry. RESULTS: Pim-1 siRNA reduces cell proliferation, induces apoptosis, causes cell cycle arrest through cell cycle related proteins (Cyclin D1 and CDK4), mitochondrial depolarization, and decreases invasive ability in SACC-83 and SACC-LM cells. Pim-1 and RUNX3 levels are significantly relevant and associated with T-stage and nerve invasion in the ACC tissues. CONCLUSIONS: This study demonstrates the oncogenic role of Pim-1 in ACC. The findings also suggest that Pim-1 may serve as a neoteric therapeutic target and potential prognostic marker for ACC cancer.
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spelling pubmed-43041902015-01-24 Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma Zhu, Xin Xu, Jia-jie Hu, Si-si Feng, Jian-guo Jiang, Lie-hao Hou, Xiu-xiu Cao, Jun Han, Jing Ling, Zhi-qiang Ge, Ming-hua J Exp Clin Cancer Res Research BACKGROUND: Pim-1 (Provirus integration site for Moloney murine leukemia virus 1) belongs to the Ser/Thr kinase family and plays a pivotal role in occurrence and development of oncogenesis. Recent studies have demonstrated that Pim-1 phosphorylates RUNX3 and alters its subcellular localization. However, few studies have concerned the implications of Pim-1 in the salivary gland adenoid cystic carcinoma (ACC). In this study, we aimed to clarify the function of Pim-1 in ACC in vitro. Meanwhile, we measured the levels of Pim-1 and RUNX3 in the ACC tissues. The correlations between Pim-1/RUNX3 levels and clinical parameters were also analyzed. METHODS: SACC-83 and SACC-LM cells were transfected with the Pim-1 siRNA. Pim-1 mRNA and protein expression were measured using real-time PCR and immnuoblot, respectively. Cell proliferation was analyzed by CCK-8 assay. Cell cycle, apoptosis, and mitochondrial membrane potential were detected by flow cytometry. Effects of Pim-1 on cells’ invasion were evaluated by transwell migration assay. Pim-1 and RUNX3 levels in ACC tissues were examined by immunohistochemistry. RESULTS: Pim-1 siRNA reduces cell proliferation, induces apoptosis, causes cell cycle arrest through cell cycle related proteins (Cyclin D1 and CDK4), mitochondrial depolarization, and decreases invasive ability in SACC-83 and SACC-LM cells. Pim-1 and RUNX3 levels are significantly relevant and associated with T-stage and nerve invasion in the ACC tissues. CONCLUSIONS: This study demonstrates the oncogenic role of Pim-1 in ACC. The findings also suggest that Pim-1 may serve as a neoteric therapeutic target and potential prognostic marker for ACC cancer. BioMed Central 2014-12-31 /pmc/articles/PMC4304190/ /pubmed/25551195 http://dx.doi.org/10.1186/s13046-014-0114-5 Text en © Zhu et al.; licensee BioMed Central. 2014 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Zhu, Xin
Xu, Jia-jie
Hu, Si-si
Feng, Jian-guo
Jiang, Lie-hao
Hou, Xiu-xiu
Cao, Jun
Han, Jing
Ling, Zhi-qiang
Ge, Ming-hua
Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma
title Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma
title_full Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma
title_fullStr Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma
title_full_unstemmed Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma
title_short Pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma
title_sort pim-1 acts as an oncogene in human salivary gland adenoid cystic carcinoma
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304190/
https://www.ncbi.nlm.nih.gov/pubmed/25551195
http://dx.doi.org/10.1186/s13046-014-0114-5
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