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Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells
In the present study, we explored the participation of Notch1 targeted regulation of mir-224/LRIG2 gene signal pathway in proliferation and apoptosis of cervical cancer cells. Forty-nine cases of cervical cancer lesion samples from cervical cancer patients treated in our hospital from February 2013...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403178/ https://www.ncbi.nlm.nih.gov/pubmed/28454395 http://dx.doi.org/10.3892/ol.2017.5676 |
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author | Cong, Lanxiang Zhang, Fang Shang, Huaihai |
author_facet | Cong, Lanxiang Zhang, Fang Shang, Huaihai |
author_sort | Cong, Lanxiang |
collection | PubMed |
description | In the present study, we explored the participation of Notch1 targeted regulation of mir-224/LRIG2 gene signal pathway in proliferation and apoptosis of cervical cancer cells. Forty-nine cases of cervical cancer lesion samples from cervical cancer patients treated in our hospital from February 2013 to February 2015 were chosen as subjects (the observation group), and cervical samples of healthy women (42 cases) during the same period were used as the control group. We determined the mRNA and protein expression of Notch1, mir-224, and LRIG2 genes. We also analyzed the mutual relationship between Notch1 gene expression and cervical cancer. The Notch1 genes in the cervical cancer cells (HeLa) were silenced and overexpressed to measure cancer apoptosis with flow cytometry. After obstruction of the Notch1 signal pathway, the mRNA and protein expression in the mir-224 and LRIG2 genes was also measured. It was found that in comparison to the control group, Notch1 gene expression in the observation group was significantly higher (p<0.05), cell growth was suppressed in Notch1 silent cell strains but accelerated in overexpressed Notch1 cells. The silencing of Notch1 genes can lead to the reduction of mir-224/LRIG gene and protein levels, while overexpression of the Notch1 genes increased the mir-224/LRIG gene and protein levels. In conclusion, the Notch1 gene is positively related to cervical cancer and can promote the occurrence of the disease. The potential mechanism shows that Notch1 gene can regulate cervical cancer cell proliferation by regulating the mir-224/LRIG2 signal pathway. |
format | Online Article Text |
id | pubmed-5403178 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-54031782017-04-27 Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells Cong, Lanxiang Zhang, Fang Shang, Huaihai Oncol Lett Articles In the present study, we explored the participation of Notch1 targeted regulation of mir-224/LRIG2 gene signal pathway in proliferation and apoptosis of cervical cancer cells. Forty-nine cases of cervical cancer lesion samples from cervical cancer patients treated in our hospital from February 2013 to February 2015 were chosen as subjects (the observation group), and cervical samples of healthy women (42 cases) during the same period were used as the control group. We determined the mRNA and protein expression of Notch1, mir-224, and LRIG2 genes. We also analyzed the mutual relationship between Notch1 gene expression and cervical cancer. The Notch1 genes in the cervical cancer cells (HeLa) were silenced and overexpressed to measure cancer apoptosis with flow cytometry. After obstruction of the Notch1 signal pathway, the mRNA and protein expression in the mir-224 and LRIG2 genes was also measured. It was found that in comparison to the control group, Notch1 gene expression in the observation group was significantly higher (p<0.05), cell growth was suppressed in Notch1 silent cell strains but accelerated in overexpressed Notch1 cells. The silencing of Notch1 genes can lead to the reduction of mir-224/LRIG gene and protein levels, while overexpression of the Notch1 genes increased the mir-224/LRIG gene and protein levels. In conclusion, the Notch1 gene is positively related to cervical cancer and can promote the occurrence of the disease. The potential mechanism shows that Notch1 gene can regulate cervical cancer cell proliferation by regulating the mir-224/LRIG2 signal pathway. D.A. Spandidos 2017-04 2017-02-03 /pmc/articles/PMC5403178/ /pubmed/28454395 http://dx.doi.org/10.3892/ol.2017.5676 Text en Copyright: © Cong et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Cong, Lanxiang Zhang, Fang Shang, Huaihai Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells |
title | Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells |
title_full | Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells |
title_fullStr | Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells |
title_full_unstemmed | Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells |
title_short | Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells |
title_sort | notch1 targeted regulation of mir-224/lrig2 signaling for the proliferation and apoptosis of cervical cancer cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403178/ https://www.ncbi.nlm.nih.gov/pubmed/28454395 http://dx.doi.org/10.3892/ol.2017.5676 |
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