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Published in: Tumor Biology 9/2016

01-09-2016 | Original Article

Overexpression of p42.3 promotes cell proliferation, migration, and invasion in human gastric cancer cells

Authors: Wen-Jia Cao, Wen-Qi Du, Lin-Lin Mao, Jun-Nian Zheng, Dong-Sheng Pei

Published in: Tumor Biology | Issue 9/2016

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Abstract

As a newly discovered tumor-specific gene, p42.3 is overexpressed in most of human gastric cancers (GC). However, the role of p42.3 in GC progression remains unclear. To assess the role of p42.3 in gastric cancers, immunohistochemistry and western blot were performed to detect the p42.3 expression in human GC tissues and cells. We also investigated the role of p42.3 in GC cell proliferation, migration, and invasion. Our results showed that the p42.3 expression was increased dramatically in human GC tissue and cells. In addition, we found that overexpression of p42.3 promotes GC cell proliferation, migration, and invasion abilities. Furthermore, p42.3 expression suppressed the E-cadherin protein level and promoted the β-catenin and p-ERK protein level. Taken together, overexpressed p42.3 is correlated with gastric cancer cell proliferation, migration, and invasion, suggesting its use as a biological marker in gastric cancer.
Literature
2.
go back to reference Li QL, Ito K, Sakakura C, Fukamachi H, Inoue K, Chi XZ, et al. Causal relationship between the loss of RUNX3 expression and gastric cancer. Cell. 2002;109:113–24.CrossRefPubMed Li QL, Ito K, Sakakura C, Fukamachi H, Inoue K, Chi XZ, et al. Causal relationship between the loss of RUNX3 expression and gastric cancer. Cell. 2002;109:113–24.CrossRefPubMed
4.
go back to reference Toyota M, Ahuja N, Suzuki H, Itoh F, Ohe-Toyota M, Imai K, et al. Aberrant methylation in gastric cancer associated with the CpG island methylator phenotype. Cancer Res. 1999;59:5438–42.PubMed Toyota M, Ahuja N, Suzuki H, Itoh F, Ohe-Toyota M, Imai K, et al. Aberrant methylation in gastric cancer associated with the CpG island methylator phenotype. Cancer Res. 1999;59:5438–42.PubMed
5.
go back to reference Xu X, Li W, Fan X, Liang Y, Zhao M, Zhang J, et al. Identification and characterization of a novel p42.3 gene as tumor-specific and mitosis phase-dependent expression in gastric cancer. Oncogene. 2007;26:7371–9. doi:10.1038/sj.onc.1210538.CrossRefPubMed Xu X, Li W, Fan X, Liang Y, Zhao M, Zhang J, et al. Identification and characterization of a novel p42.3 gene as tumor-specific and mitosis phase-dependent expression in gastric cancer. Oncogene. 2007;26:7371–9. doi:10.​1038/​sj.​onc.​1210538.CrossRefPubMed
9.
go back to reference Weng YR, Yu YN, Ren LL, Cui Y, Lu YY, Chen HY, et al. Role of C9orf140 in the promotion of colorectal cancer progression and mechanisms of its upregulation via activation of STAT5, beta-catenin and EZH2. Carcinogenesis. 2014;35:1389–98. doi:10.1093/carcin/bgu057.CrossRefPubMed Weng YR, Yu YN, Ren LL, Cui Y, Lu YY, Chen HY, et al. Role of C9orf140 in the promotion of colorectal cancer progression and mechanisms of its upregulation via activation of STAT5, beta-catenin and EZH2. Carcinogenesis. 2014;35:1389–98. doi:10.​1093/​carcin/​bgu057.CrossRefPubMed
11.
go back to reference Strausberg RL, Feingold EA, Grouse LH, Derge JG, Klausner RD, Collins FS, et al. Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proc Natl Acad Sci U S A. 2002;99:16899–903. doi:10.1073/pnas.242603899.CrossRefPubMed Strausberg RL, Feingold EA, Grouse LH, Derge JG, Klausner RD, Collins FS, et al. Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proc Natl Acad Sci U S A. 2002;99:16899–903. doi:10.​1073/​pnas.​242603899.CrossRefPubMed
13.
go back to reference Mao L, Sun W, Li W, Cui J, Zhang J, Xing R, et al. Cell cycle-dependent expression of p42.3 promotes mitotic progression in malignant transformed cells. Mol Carcinog. 2014;53:337–48. doi:10.1002/mc.21982.CrossRefPubMed Mao L, Sun W, Li W, Cui J, Zhang J, Xing R, et al. Cell cycle-dependent expression of p42.3 promotes mitotic progression in malignant transformed cells. Mol Carcinog. 2014;53:337–48. doi:10.​1002/​mc.​21982.CrossRefPubMed
14.
24.
go back to reference Javle MM, Gibbs JF, Iwata KK, Pak Y, Rutledge P, Yu J, et al. Epithelial-mesenchymal transition (EMT) and activated extracellular signal-regulated kinase (p-Erk) in surgically resected pancreatic cancer. Ann Surg Oncol. 2007;14:3527–33. doi:10.1245/s10434-007-9540-3.CrossRefPubMed Javle MM, Gibbs JF, Iwata KK, Pak Y, Rutledge P, Yu J, et al. Epithelial-mesenchymal transition (EMT) and activated extracellular signal-regulated kinase (p-Erk) in surgically resected pancreatic cancer. Ann Surg Oncol. 2007;14:3527–33. doi:10.​1245/​s10434-007-9540-3.CrossRefPubMed
Metadata
Title
Overexpression of p42.3 promotes cell proliferation, migration, and invasion in human gastric cancer cells
Authors
Wen-Jia Cao
Wen-Qi Du
Lin-Lin Mao
Jun-Nian Zheng
Dong-Sheng Pei
Publication date
01-09-2016
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 9/2016
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-016-5242-4

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