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Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models
Ovarian cancer is the leading cause of mortality resulting from gynecologic cancer. A common anti-ovarian tumor drug is cisplatin; however, repeated use of cisplatin causes severe resistance and leads to poor long-term survival rate in ovarian cancer patients. Recently, it was reported that lanthanu...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090291/ https://www.ncbi.nlm.nih.gov/pubmed/30116365 http://dx.doi.org/10.3892/etm.2018.6299 |
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author | Wang, Fen Zhu, Yuanfang Fang, Shanyu Li, Shuya Liu, Sisun |
author_facet | Wang, Fen Zhu, Yuanfang Fang, Shanyu Li, Shuya Liu, Sisun |
author_sort | Wang, Fen |
collection | PubMed |
description | Ovarian cancer is the leading cause of mortality resulting from gynecologic cancer. A common anti-ovarian tumor drug is cisplatin; however, repeated use of cisplatin causes severe resistance and leads to poor long-term survival rate in ovarian cancer patients. Recently, it was reported that lanthanum chloride (LaCl(3)) may inhibit tumor growth and induce apoptosis in certain cancer cells. In the present study, the effect of LaCl(3) on ovarian cancer was determined in vivo and in vitro. A cisplatin-sensitive human ovarian cancer cell line, COC1, was used in the current study. A xenograft animal model of ovarian cancer was established injecting COC1 or cisplatin-resistant COC1 cells (COC1/DDP) cells into mice. A TUNEL assay was used to determine the apoptosis of the COC1 or COC1/DDP cells and a immunohistochemical assay was conducted to measure the expression of B-cell lymphoma-2, Ki67, breast cancer 1 (BRCA)1, BRCA2 and excision repair cross-complementation group 1 in COC1 or COC1/DDP cells. It was observed that LaCl(3) promoted apoptosis in COC1 and COC1/DDP cells. In addition, LaCl(3) plus cisplatin led to further increase in the expression levels of tumor suppressor genes and decrease in the expression of oncogenes. Furthermore, application of LaCl(3) and cisplatin inhibited tumor growth in vivo in a xenograft animal model. These results indicated the synergistic role of LaCl(3) on cisplatin-induced inhibition of cancer cell proliferation and tumor growth, providing a potential and effective candidate for the treatment of ovarian tumors. |
format | Online Article Text |
id | pubmed-6090291 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-60902912018-08-16 Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models Wang, Fen Zhu, Yuanfang Fang, Shanyu Li, Shuya Liu, Sisun Exp Ther Med Articles Ovarian cancer is the leading cause of mortality resulting from gynecologic cancer. A common anti-ovarian tumor drug is cisplatin; however, repeated use of cisplatin causes severe resistance and leads to poor long-term survival rate in ovarian cancer patients. Recently, it was reported that lanthanum chloride (LaCl(3)) may inhibit tumor growth and induce apoptosis in certain cancer cells. In the present study, the effect of LaCl(3) on ovarian cancer was determined in vivo and in vitro. A cisplatin-sensitive human ovarian cancer cell line, COC1, was used in the current study. A xenograft animal model of ovarian cancer was established injecting COC1 or cisplatin-resistant COC1 cells (COC1/DDP) cells into mice. A TUNEL assay was used to determine the apoptosis of the COC1 or COC1/DDP cells and a immunohistochemical assay was conducted to measure the expression of B-cell lymphoma-2, Ki67, breast cancer 1 (BRCA)1, BRCA2 and excision repair cross-complementation group 1 in COC1 or COC1/DDP cells. It was observed that LaCl(3) promoted apoptosis in COC1 and COC1/DDP cells. In addition, LaCl(3) plus cisplatin led to further increase in the expression levels of tumor suppressor genes and decrease in the expression of oncogenes. Furthermore, application of LaCl(3) and cisplatin inhibited tumor growth in vivo in a xenograft animal model. These results indicated the synergistic role of LaCl(3) on cisplatin-induced inhibition of cancer cell proliferation and tumor growth, providing a potential and effective candidate for the treatment of ovarian tumors. D.A. Spandidos 2018-08 2018-06-13 /pmc/articles/PMC6090291/ /pubmed/30116365 http://dx.doi.org/10.3892/etm.2018.6299 Text en Copyright: © Wang 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 Wang, Fen Zhu, Yuanfang Fang, Shanyu Li, Shuya Liu, Sisun Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models |
title | Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models |
title_full | Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models |
title_fullStr | Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models |
title_full_unstemmed | Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models |
title_short | Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models |
title_sort | effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090291/ https://www.ncbi.nlm.nih.gov/pubmed/30116365 http://dx.doi.org/10.3892/etm.2018.6299 |
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