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Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition
Thyroid cancer is maintaining at a high incidence level and its carcinogenesis is mainly affected by a complex gene interaction. By analysis of the next‐generation resequencing of paired papillary thyroid cancer (PTC) and adjacent thyroid tissues, we found that Growth Associated Protein 43 (GAP43),...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850924/ https://www.ncbi.nlm.nih.gov/pubmed/31568662 http://dx.doi.org/10.1111/jcmm.14460 |
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author | Zheng, Chen Quan, Rui‐Da Wu, Cheng‐Yong Hu, Jing Lin, Bang‐Yi Dong, Xu‐Bing Xia, Er‐Jie Bhandari, Adheesh Zhang, Xiao‐Hua Wang, Ou‐Chen |
author_facet | Zheng, Chen Quan, Rui‐Da Wu, Cheng‐Yong Hu, Jing Lin, Bang‐Yi Dong, Xu‐Bing Xia, Er‐Jie Bhandari, Adheesh Zhang, Xiao‐Hua Wang, Ou‐Chen |
author_sort | Zheng, Chen |
collection | PubMed |
description | Thyroid cancer is maintaining at a high incidence level and its carcinogenesis is mainly affected by a complex gene interaction. By analysis of the next‐generation resequencing of paired papillary thyroid cancer (PTC) and adjacent thyroid tissues, we found that Growth Associated Protein 43 (GAP43), a phosphoprotein activated by protein kinase C, might be novel markers associated with PTC. However, its function in thyroid carcinoma has been poorly understood. We discovered that GAP43 was significantly overexpressed in thyroid carcinoma and these results were consistent with that in The Cancer Genome Atlas (TCGA) cohort. In addition, some clinicopathological features of GAP43 in TCGA database showed that up‐regulated GAP43 is significantly connected to lymph node metastasis (P < 0.001) and tumour size (P = 0.038). In vitro experiments, loss of function experiments was performed to investigate GAP43 in PTC cell lines (TPC‐1 and BCPAP). The results proved that GAP43 knockdown in PTC cell significantly decreased the function of cell proliferation, colony formation, migration, and invasion and induced cell apoptosis. Furthermore, we also indicated that GAP43 could modulate the expression of epithelial‐mesenchymal transition‐related proteins, which could influence invasion and migration. Put those results together, GAP43 is a gene which was associated with PTC and might be a potential therapeutic target. |
format | Online Article Text |
id | pubmed-6850924 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68509242019-12-01 Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition Zheng, Chen Quan, Rui‐Da Wu, Cheng‐Yong Hu, Jing Lin, Bang‐Yi Dong, Xu‐Bing Xia, Er‐Jie Bhandari, Adheesh Zhang, Xiao‐Hua Wang, Ou‐Chen J Cell Mol Med Original Articles Thyroid cancer is maintaining at a high incidence level and its carcinogenesis is mainly affected by a complex gene interaction. By analysis of the next‐generation resequencing of paired papillary thyroid cancer (PTC) and adjacent thyroid tissues, we found that Growth Associated Protein 43 (GAP43), a phosphoprotein activated by protein kinase C, might be novel markers associated with PTC. However, its function in thyroid carcinoma has been poorly understood. We discovered that GAP43 was significantly overexpressed in thyroid carcinoma and these results were consistent with that in The Cancer Genome Atlas (TCGA) cohort. In addition, some clinicopathological features of GAP43 in TCGA database showed that up‐regulated GAP43 is significantly connected to lymph node metastasis (P < 0.001) and tumour size (P = 0.038). In vitro experiments, loss of function experiments was performed to investigate GAP43 in PTC cell lines (TPC‐1 and BCPAP). The results proved that GAP43 knockdown in PTC cell significantly decreased the function of cell proliferation, colony formation, migration, and invasion and induced cell apoptosis. Furthermore, we also indicated that GAP43 could modulate the expression of epithelial‐mesenchymal transition‐related proteins, which could influence invasion and migration. Put those results together, GAP43 is a gene which was associated with PTC and might be a potential therapeutic target. John Wiley and Sons Inc. 2019-09-30 2019-12 /pmc/articles/PMC6850924/ /pubmed/31568662 http://dx.doi.org/10.1111/jcmm.14460 Text en © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Zheng, Chen Quan, Rui‐Da Wu, Cheng‐Yong Hu, Jing Lin, Bang‐Yi Dong, Xu‐Bing Xia, Er‐Jie Bhandari, Adheesh Zhang, Xiao‐Hua Wang, Ou‐Chen Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition |
title | Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition |
title_full | Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition |
title_fullStr | Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition |
title_full_unstemmed | Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition |
title_short | Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition |
title_sort | growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850924/ https://www.ncbi.nlm.nih.gov/pubmed/31568662 http://dx.doi.org/10.1111/jcmm.14460 |
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