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Nonylphenol promotes the proliferation of colorectal cancer COLO205 cells by upregulating the expression of protein kinase C ζ

Authors
  • Yang, Xuefeng1
  • Huang, Handong1
  • Wang, Maijian1
  • Zheng, Xingbin1
  • Xie, Ming1
  • Xu, Jie2
  • 1 Department of Gastrointestinal Surgery, Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563000, P.R. China
  • 2 School of Public Health, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China
Type
Published Article
Journal
Oncology Letters
Publisher
Spandidos Publications
Publication Date
Dec 18, 2018
Volume
17
Issue
2
Pages
2498–2506
Identifiers
DOI: 10.3892/ol.2018.9846
PMID: 30675313
PMCID: PMC6341561
Source
PubMed Central
Keywords
License
Unknown

Abstract

Previous studies have indicated the potential role of estrogen in the development and prognosis of colorectal cancer (CRC). Nonylpheno (NP) is an endocrine-disrupting chemical, which may influence the development of estrogen-dependent types of cancer. However, the molecular mechanism of NP in the development of CRCs remains unclear. In the present study, various concentrations of NP were used to treat COLO205 CRC cells, and the expression of protein kinase C ζ (PKCζ) was knocked down using PKCζ small interfering RNA. The effects of NP in various concentrations on the cell cycle and apoptosis of COLO205 cells were examined, and the change in the expression level of PKCζ was analyzed. The results indicated that NP may significantly induce proliferation of COLO205 CRC cells, and significantly reduce cell apoptosis. However, suppression of PKCζ expression may inhibit proliferation, while NP could reduce this inhibition. The results of a western blot analysis indicated that the expression level of cyclin D1 and E were significantly increased following NP treatment, and the expression of p27 was significantly decreased. The phosphorylation of PKCζ and extracellular-signal-regulated kinase (ERK)1/2 was significantly increased following NP treatment in a dose-dependent manner. Overall, NP induced human CRC COLO205 cell proliferation and inhibited the apoptotic rate of COLO205 cells by increasing the activity of PKCζ and ERK1/2.

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