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MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells

BACKGROUND: Melanoma is notoriously resistant to all current modalities of cancer therapies including chemotherapy. In recent years, microRNAs (miRNAs) have emerged as molecular regulators in the development and progression of melanoma. However, the relationship between microRNA and chemo-resistance...

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Autores principales: Li, Yuxia, Zhang, Jie, Liu, Yajing, Zhang, Bingyue, Zhong, Fubo, Wang, Shubin, Fang, Zhengyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896053/
https://www.ncbi.nlm.nih.gov/pubmed/29642855
http://dx.doi.org/10.1186/s12885-018-4233-9
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author Li, Yuxia
Zhang, Jie
Liu, Yajing
Zhang, Bingyue
Zhong, Fubo
Wang, Shubin
Fang, Zhengyu
author_facet Li, Yuxia
Zhang, Jie
Liu, Yajing
Zhang, Bingyue
Zhong, Fubo
Wang, Shubin
Fang, Zhengyu
author_sort Li, Yuxia
collection PubMed
description BACKGROUND: Melanoma is notoriously resistant to all current modalities of cancer therapies including chemotherapy. In recent years, microRNAs (miRNAs) have emerged as molecular regulators in the development and progression of melanoma. However, the relationship between microRNA and chemo-resistance of melanoma is little known. In present study, we aimed to investigate the miRNAs related to cisplatin-resistance in melanoma cells. METHODS: After cisplatin (DDP) resistant melanoma cells (M8/DDP and SK-Mel-19/DDP) were established in-vitro, high-throughput screening of differentially expressed miRNAs between resistant cells and parental cells were performed. RESULTS: It was found that a cancer-related miRNA, miR-30a-5p, was highly over-expressed in resistant cells. Transfection of miR-30a-5p mimic or inhibitor could alter the sensitivity of melanoma cells to cisplatin. Next, we showed that Insulin Like Growth Factor 1 Receptor (IGF1R) gene turned out to be a direct target of miR-30a-5p. Knockdown of IGF1R in melanoma cells could not only reduce the sensitivity to cisplatin but also lead to cell cycle arrest by regulating phosphorylation of Serine-Threonine Protein Kinase (P-AKT (Ser473)) and Tumor Protein P53 (P53). CONCLUSION: Taken together, our study demonstrated that miR-30a-5p could influence chemo-resistance by targeting IGF1R gene in melanoma cells, which might provide a potential target for the therapy of chemo-resistant melanoma cells.
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spelling pubmed-58960532018-04-12 MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells Li, Yuxia Zhang, Jie Liu, Yajing Zhang, Bingyue Zhong, Fubo Wang, Shubin Fang, Zhengyu BMC Cancer Research Article BACKGROUND: Melanoma is notoriously resistant to all current modalities of cancer therapies including chemotherapy. In recent years, microRNAs (miRNAs) have emerged as molecular regulators in the development and progression of melanoma. However, the relationship between microRNA and chemo-resistance of melanoma is little known. In present study, we aimed to investigate the miRNAs related to cisplatin-resistance in melanoma cells. METHODS: After cisplatin (DDP) resistant melanoma cells (M8/DDP and SK-Mel-19/DDP) were established in-vitro, high-throughput screening of differentially expressed miRNAs between resistant cells and parental cells were performed. RESULTS: It was found that a cancer-related miRNA, miR-30a-5p, was highly over-expressed in resistant cells. Transfection of miR-30a-5p mimic or inhibitor could alter the sensitivity of melanoma cells to cisplatin. Next, we showed that Insulin Like Growth Factor 1 Receptor (IGF1R) gene turned out to be a direct target of miR-30a-5p. Knockdown of IGF1R in melanoma cells could not only reduce the sensitivity to cisplatin but also lead to cell cycle arrest by regulating phosphorylation of Serine-Threonine Protein Kinase (P-AKT (Ser473)) and Tumor Protein P53 (P53). CONCLUSION: Taken together, our study demonstrated that miR-30a-5p could influence chemo-resistance by targeting IGF1R gene in melanoma cells, which might provide a potential target for the therapy of chemo-resistant melanoma cells. BioMed Central 2018-04-11 /pmc/articles/PMC5896053/ /pubmed/29642855 http://dx.doi.org/10.1186/s12885-018-4233-9 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Li, Yuxia
Zhang, Jie
Liu, Yajing
Zhang, Bingyue
Zhong, Fubo
Wang, Shubin
Fang, Zhengyu
MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells
title MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells
title_full MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells
title_fullStr MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells
title_full_unstemmed MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells
title_short MiR-30a-5p confers cisplatin resistance by regulating IGF1R expression in melanoma cells
title_sort mir-30a-5p confers cisplatin resistance by regulating igf1r expression in melanoma cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896053/
https://www.ncbi.nlm.nih.gov/pubmed/29642855
http://dx.doi.org/10.1186/s12885-018-4233-9
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