Article
17-beta Estradiol increases Connexin43 expression on F-98 rat glioma cell line
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Authors
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Zahra Moinfar
- Ruhr University Bochum, Neuroanatomy and Molecular Brain Research, Bochum, Germany; International Graduate School of Neuroscience (IGSN), Neuroanatomy and Molecular Brain Research, Bochum, Germany
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Fatme Seval Ismail
- Ruhr University Bochum, Neuroanatomy and Molecular Brain Research, Bochum, Germany
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Hannes Dambach
- Ruhr University Bochum, Neuroanatomy and Molecular Brain Research, Bochum, Germany
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Daniel Hinkerohe
- Ruhr University Bochum, Department of Neurology, knappschafts hospital, Bochum, Germany
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Ralf Gold
- International Graduate School of Neuroscience (IGSN), Department of Neurology, St. Josef Hospital, Bochum, Germany; Ruhr University Bochum, Department of Neurology, St. Josef Hospital, Bochum, Germany
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Pedro Michael Faustmann
- Ruhr University Bochum, Neuroanatomy and Molecular Brain Research, Bochum, Germany; International Graduate School of Neuroscience (IGSN), Neuroanatomy and Molecular Brain Research, Bochum, Germany
| Published: | September 11, 2012 |
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Outline
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Question: Glioblastoma is the most aggressive form of primary brain tumor with the male preponderance (male:female=2:1) but few studies have addressed the sex hormone effects. Cell-cell communication is one of the important features for maintaining cell growth and proliferation in tumor cells. Similarly, gap junctions (GJ) are important means for cellular communications and Connexin 43 (Cx43) is the most abundant GJ on astrocytes, the origine of glioblastomas. Thus study of the effect of 17-beta Estradiol (Es) on pathology, progression and therapeutic means might be of therapeutic relevance. Consequently, we evaluated the effect of 17-beta Estradiol on Cx43 on F-98 rat glioma cell lines.
Methods: F-98 cell lines were cultured on PLL coated coverslips on either 24 well-plates or Petri dishes by 40,000/well. Immunohistochemistry (IHC) and Western Blotting (WB) for Cx43 were performed after 24hr/7day incubations with 100nM of 17-beta Estradiol (Es). All experiments were repeated at least 4 times from separate cell cultures. The data was analyzed with GraphPad Prism version 5.04 using Mann-Whitney test and was considered significant with Pvalue
Results: F-98 cells showed increased expression of Cx43 from 100% to 123.3% ±11.14 (Mean±SEM) (Pvalue=0.007) in 24 hours incubation. Furthermore, they showed increased expression by 219.8%±35.61 (Mean±SEM) (Pvalue=0.01) in 7-day incubation with estradiol as well.
Conclusions: The increased expression of Cx43 has been reported in the human biopsies of gliomas and over- expression had inverse association with the grade of the tumors. Similarly, estradiol increased the survival in the glioma-induced rats. However, whether manipulation of Cx43 is beneficial for tumor growth is still unknown. One hypothesis suggests that higher expression of Cx43 can help immune cells to recognize the tumor antigens to detect and eliminate the tumor cells. Also, Cx43 is responsive to Es and it has been shown it can functions as tumor suppressor genes as well. As to our knowledge, this is the first report of sex steroid hormone modulation of Cx43 in the tumor cells which is in favor of the beneficial role of Es on tumor cells. We suggest investigating the role of Es on the tumor adhesive molecules with another cell line as well to further understand the role of Es on Cx43.
