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Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling

Remodeling and spacing factor 1 (Rsf-1) has been reported as overexpressed in numerous cancers; however, its expression, biological functions and mechanisms in malignant melanoma remain unknown. In the present study, the expression of Rsf-1 was investigated in 50 cases of malignant melanoma samples...

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Autores principales: He, Jiani, Fu, Lin, Li, Qingchang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755232/
https://www.ncbi.nlm.nih.gov/pubmed/31485613
http://dx.doi.org/10.3892/mmr.2019.10610
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author He, Jiani
Fu, Lin
Li, Qingchang
author_facet He, Jiani
Fu, Lin
Li, Qingchang
author_sort He, Jiani
collection PubMed
description Remodeling and spacing factor 1 (Rsf-1) has been reported as overexpressed in numerous cancers; however, its expression, biological functions and mechanisms in malignant melanoma remain unknown. In the present study, the expression of Rsf-1 was investigated in 50 cases of malignant melanoma samples using immunohistochemistry. The results revealed that Rsf-1 expression was elevated in 38% of specimens. MTT, colony formation, Transwell and flow cytometry assays were performed to investigate the functions of Rsf-1. Knockdown of Rsf-1 in the MV3 and A375 melanoma cell lines decreased the viability, invasion and cell cycle transition of cells. Conversely, overexpression of Rsf-1 in M14 cells with low endogenous Rsf-1 expression induced opposing effects. Further analysis revealed that Rsf-1 knockdown decreased matrix metalloproteinase-2, cyclin E and phosphorylated-IκB expression. Additionally, Rsf-1 depletion reduced cisplatin resistance and significantly increased the cisplatin-associated apoptotic rate, whereas Rsf-1 overexpression exhibited opposing effects. Rsf-1 also maintained the mitochondrial membrane potential following cisplatin treatment. Analysis of apoptosis-associated proteins revealed that Rsf-1 positively regulated B-cell lymphoma 2 (Bcl-2), cellular inhibitor of apoptosis 1 (cIAP1) and cIAP2, and downregulated Bcl-2-associated X protein expression. Nuclear factor κ-light-chain-enhancer of activated B-cells (NF-κB) inhibition reversed the effects of Rsf-1 on Bcl-2. In conclusion, Rsf-1 was overexpressed in malignant melanoma and may contribute to the malignant behaviors of melanoma cells, possibly via the regulation of NF-κB signaling. Therefore, Rsf-1 may be a potential therapeutic target in the treatment of malignant melanoma.
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spelling pubmed-67552322019-09-25 Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling He, Jiani Fu, Lin Li, Qingchang Mol Med Rep Articles Remodeling and spacing factor 1 (Rsf-1) has been reported as overexpressed in numerous cancers; however, its expression, biological functions and mechanisms in malignant melanoma remain unknown. In the present study, the expression of Rsf-1 was investigated in 50 cases of malignant melanoma samples using immunohistochemistry. The results revealed that Rsf-1 expression was elevated in 38% of specimens. MTT, colony formation, Transwell and flow cytometry assays were performed to investigate the functions of Rsf-1. Knockdown of Rsf-1 in the MV3 and A375 melanoma cell lines decreased the viability, invasion and cell cycle transition of cells. Conversely, overexpression of Rsf-1 in M14 cells with low endogenous Rsf-1 expression induced opposing effects. Further analysis revealed that Rsf-1 knockdown decreased matrix metalloproteinase-2, cyclin E and phosphorylated-IκB expression. Additionally, Rsf-1 depletion reduced cisplatin resistance and significantly increased the cisplatin-associated apoptotic rate, whereas Rsf-1 overexpression exhibited opposing effects. Rsf-1 also maintained the mitochondrial membrane potential following cisplatin treatment. Analysis of apoptosis-associated proteins revealed that Rsf-1 positively regulated B-cell lymphoma 2 (Bcl-2), cellular inhibitor of apoptosis 1 (cIAP1) and cIAP2, and downregulated Bcl-2-associated X protein expression. Nuclear factor κ-light-chain-enhancer of activated B-cells (NF-κB) inhibition reversed the effects of Rsf-1 on Bcl-2. In conclusion, Rsf-1 was overexpressed in malignant melanoma and may contribute to the malignant behaviors of melanoma cells, possibly via the regulation of NF-κB signaling. Therefore, Rsf-1 may be a potential therapeutic target in the treatment of malignant melanoma. D.A. Spandidos 2019-10 2019-08-23 /pmc/articles/PMC6755232/ /pubmed/31485613 http://dx.doi.org/10.3892/mmr.2019.10610 Text en Copyright: © He 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
He, Jiani
Fu, Lin
Li, Qingchang
Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling
title Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling
title_full Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling
title_fullStr Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling
title_full_unstemmed Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling
title_short Rsf-1 regulates malignant melanoma cell viability and chemoresistance via NF-κB/Bcl-2 signaling
title_sort rsf-1 regulates malignant melanoma cell viability and chemoresistance via nf-κb/bcl-2 signaling
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755232/
https://www.ncbi.nlm.nih.gov/pubmed/31485613
http://dx.doi.org/10.3892/mmr.2019.10610
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