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Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271
OBJECTIVE: Cancer metastasis remains the primary cause of cancer-related death worldwide. In a previous study, we found that levels of BTB/POZ domain-containing protein KCTD12 are lower in metastatic melanoma cells than in parental melanoma cells. The purpose of this study was to identify the roles...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Chinese Anti-Cancer Association
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6743620/ https://www.ncbi.nlm.nih.gov/pubmed/31565480 http://dx.doi.org/10.20892/j.issn.2095-3941.2019.0073 |
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author | Shen, Weiyu Li, Yumei Li, Bifei Zheng, Liping Xie, Xiaodong Le, Jingqing Lu, Yusheng Li, Tao Chen, Fan Jia, Lee |
author_facet | Shen, Weiyu Li, Yumei Li, Bifei Zheng, Liping Xie, Xiaodong Le, Jingqing Lu, Yusheng Li, Tao Chen, Fan Jia, Lee |
author_sort | Shen, Weiyu |
collection | PubMed |
description | OBJECTIVE: Cancer metastasis remains the primary cause of cancer-related death worldwide. In a previous study, we found that levels of BTB/POZ domain-containing protein KCTD12 are lower in metastatic melanoma cells than in parental melanoma cells. The purpose of this study was to identify the roles of KCTD12 in cancer metastasis. METHODS: The Cancer Genome Atlas (TCGA) datasets were used to evaluate the relationship between KCTD12 and skin cutaneous melanoma (SKCM) prognosis. The effects of endogenous KCTD12 on biological behaviors were examined using the MTT assay. The impacts of KCTD12 on melanoma stemness were explored using spheroid formation assay. KCTD12 knockout A375 cells were generated to confirm the inhibitory effect of KCTD12 on CD271, and a mouse metastatic model was used to determine the impact of KCTD12 on melanoma metastasis in vivo. RESULTS: KCTD12 levels were lower in lung metastatic cells than in paired parental melanoma cells, and low KCTD12 expression indicated a poor prognosis in SKCM. Cancer metastasis-related capacities were higher in lung metastatic cells than in parental melanoma cells. Moreover, KCTD12 knockdown enhanced tumor growth and metastasis both in vitro and in vivo. Mechanistically, the interaction between KCTD12 and CD271 might be responsible for the stemness transformation after KCTD12 knockdown. CONCLUSIONS: This study identifies for the first time the role of the interaction between KCTD12 and CD271 in inducing melanoma cell stemness transformation. Moreover, KCTD12 repression enhances melanoma cell growth, adhesion, migration and invasion. |
format | Online Article Text |
id | pubmed-6743620 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Chinese Anti-Cancer Association |
record_format | MEDLINE/PubMed |
spelling | pubmed-67436202019-09-27 Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271 Shen, Weiyu Li, Yumei Li, Bifei Zheng, Liping Xie, Xiaodong Le, Jingqing Lu, Yusheng Li, Tao Chen, Fan Jia, Lee Cancer Biol Med Original Article OBJECTIVE: Cancer metastasis remains the primary cause of cancer-related death worldwide. In a previous study, we found that levels of BTB/POZ domain-containing protein KCTD12 are lower in metastatic melanoma cells than in parental melanoma cells. The purpose of this study was to identify the roles of KCTD12 in cancer metastasis. METHODS: The Cancer Genome Atlas (TCGA) datasets were used to evaluate the relationship between KCTD12 and skin cutaneous melanoma (SKCM) prognosis. The effects of endogenous KCTD12 on biological behaviors were examined using the MTT assay. The impacts of KCTD12 on melanoma stemness were explored using spheroid formation assay. KCTD12 knockout A375 cells were generated to confirm the inhibitory effect of KCTD12 on CD271, and a mouse metastatic model was used to determine the impact of KCTD12 on melanoma metastasis in vivo. RESULTS: KCTD12 levels were lower in lung metastatic cells than in paired parental melanoma cells, and low KCTD12 expression indicated a poor prognosis in SKCM. Cancer metastasis-related capacities were higher in lung metastatic cells than in parental melanoma cells. Moreover, KCTD12 knockdown enhanced tumor growth and metastasis both in vitro and in vivo. Mechanistically, the interaction between KCTD12 and CD271 might be responsible for the stemness transformation after KCTD12 knockdown. CONCLUSIONS: This study identifies for the first time the role of the interaction between KCTD12 and CD271 in inducing melanoma cell stemness transformation. Moreover, KCTD12 repression enhances melanoma cell growth, adhesion, migration and invasion. Chinese Anti-Cancer Association 2019-08 /pmc/articles/PMC6743620/ /pubmed/31565480 http://dx.doi.org/10.20892/j.issn.2095-3941.2019.0073 Text en Copyright 2019 Cancer Biology & Medicine http://creativecommons.org/licenses/by-nc-sa/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-Share Alike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/ |
spellingShingle | Original Article Shen, Weiyu Li, Yumei Li, Bifei Zheng, Liping Xie, Xiaodong Le, Jingqing Lu, Yusheng Li, Tao Chen, Fan Jia, Lee Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271 |
title | Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271 |
title_full | Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271 |
title_fullStr | Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271 |
title_full_unstemmed | Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271 |
title_short | Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271 |
title_sort | downregulation of kctd12 contributes to melanoma stemness by modulating cd271 |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6743620/ https://www.ncbi.nlm.nih.gov/pubmed/31565480 http://dx.doi.org/10.20892/j.issn.2095-3941.2019.0073 |
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