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Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer
Cisplatin (DDP) chemotherapy is the primary modality of treatment for non-small cell lung cancer (NSCLC). However, due to the occurrence of DDP resistance, only a limited number of patients benefit from this treatment regimen. Brother of Regulator of Imprinted Sites (BORIS) is expressed elevated in...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7509674/ https://www.ncbi.nlm.nih.gov/pubmed/32994814 http://dx.doi.org/10.3892/ol.2020.12114 |
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author | Zhang, Yanmei Song, Yongfei Li, Chao Ren, Juan Fang, Mengdie Fang, Jianfei Wang, Xiaoju |
author_facet | Zhang, Yanmei Song, Yongfei Li, Chao Ren, Juan Fang, Mengdie Fang, Jianfei Wang, Xiaoju |
author_sort | Zhang, Yanmei |
collection | PubMed |
description | Cisplatin (DDP) chemotherapy is the primary modality of treatment for non-small cell lung cancer (NSCLC). However, due to the occurrence of DDP resistance, only a limited number of patients benefit from this treatment regimen. Brother of Regulator of Imprinted Sites (BORIS) is expressed elevated in NSCLC. Whether BORIS is involved in the DDP resistance of NSCLC is currently undetermined. The association between BORIS expression and overall survival rate of 156 patients with NSCLC who received DDP chemotherapy was analyzed in the present study. In order to investigate the function of BORIS in DDP chemotherapy, BORIS was silenced or overexpressed in four NSCLC cell lines. The cell viabilities, apoptosis and DNA damage induced by DDP were evaluated in these cell lines. In addition, the regulations of DNA repair genes were assessed, including POLH, ERCC1, BRCA1, MSH6 and XPA. The present study demonstrated that high BORIS expression was associated with decreased overall survival rate in patients with NSCLC who received DDP chemotherapy. The patients who benefited and went into remission following DDP therapy expressed a relatively low level of BORIS, suggesting the potential function of BORIS in DDP resistance. Cell experiments revealed that NSCLC cells that had a higher proliferation rate and resisted DDP treatment expressed a relatively higher level of BORIS. Knockdown of BORIS in NSCLC cells induced DNA damage; inhibiting cell proliferation and sensitizing cells to DDP treatment. In contrast, BORIS overexpression suppressed DDP-induced DNA damage. Notably, the mismatch repair factor mutS homolog 6 (MSH6) was regulated by BORIS, indicating its association with BORIS-associated DDP resistance in NSCLC. The findings of the present study suggest that BORIS suppresses DNA damage and promotes the progression of NSCLC and DDP resistance. The present study indicates the potential application of BORIS in NSCLC therapy and prognosis. |
format | Online Article Text |
id | pubmed-7509674 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-75096742020-09-28 Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer Zhang, Yanmei Song, Yongfei Li, Chao Ren, Juan Fang, Mengdie Fang, Jianfei Wang, Xiaoju Oncol Lett Articles Cisplatin (DDP) chemotherapy is the primary modality of treatment for non-small cell lung cancer (NSCLC). However, due to the occurrence of DDP resistance, only a limited number of patients benefit from this treatment regimen. Brother of Regulator of Imprinted Sites (BORIS) is expressed elevated in NSCLC. Whether BORIS is involved in the DDP resistance of NSCLC is currently undetermined. The association between BORIS expression and overall survival rate of 156 patients with NSCLC who received DDP chemotherapy was analyzed in the present study. In order to investigate the function of BORIS in DDP chemotherapy, BORIS was silenced or overexpressed in four NSCLC cell lines. The cell viabilities, apoptosis and DNA damage induced by DDP were evaluated in these cell lines. In addition, the regulations of DNA repair genes were assessed, including POLH, ERCC1, BRCA1, MSH6 and XPA. The present study demonstrated that high BORIS expression was associated with decreased overall survival rate in patients with NSCLC who received DDP chemotherapy. The patients who benefited and went into remission following DDP therapy expressed a relatively low level of BORIS, suggesting the potential function of BORIS in DDP resistance. Cell experiments revealed that NSCLC cells that had a higher proliferation rate and resisted DDP treatment expressed a relatively higher level of BORIS. Knockdown of BORIS in NSCLC cells induced DNA damage; inhibiting cell proliferation and sensitizing cells to DDP treatment. In contrast, BORIS overexpression suppressed DDP-induced DNA damage. Notably, the mismatch repair factor mutS homolog 6 (MSH6) was regulated by BORIS, indicating its association with BORIS-associated DDP resistance in NSCLC. The findings of the present study suggest that BORIS suppresses DNA damage and promotes the progression of NSCLC and DDP resistance. The present study indicates the potential application of BORIS in NSCLC therapy and prognosis. D.A. Spandidos 2020-11 2020-09-17 /pmc/articles/PMC7509674/ /pubmed/32994814 http://dx.doi.org/10.3892/ol.2020.12114 Text en Copyright: © Zhang 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 Zhang, Yanmei Song, Yongfei Li, Chao Ren, Juan Fang, Mengdie Fang, Jianfei Wang, Xiaoju Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer |
title | Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer |
title_full | Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer |
title_fullStr | Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer |
title_full_unstemmed | Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer |
title_short | Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer |
title_sort | brother of regulator of imprinted sites inhibits cisplatin-induced dna damage in non-small cell lung cancer |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7509674/ https://www.ncbi.nlm.nih.gov/pubmed/32994814 http://dx.doi.org/10.3892/ol.2020.12114 |
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