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The role of DYNLT3 in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition
PURPOSE: DYNLT3 is identified as an age‐related gene. Nevertheless, the specific mechanism of its carcinogenesis in breast tumor has not been clarified. This research aims to elucidate the role and the underlying molecular pathways of DYNLT3 on breast cancer tumorigenesis. METHODS: The differential...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10417059/ https://www.ncbi.nlm.nih.gov/pubmed/37260179 http://dx.doi.org/10.1002/cam4.6173 |
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author | Wang, Han Chen, Xin Jin, Yanshan Liu, Tingxian Song, Yizuo Zhu, Xuejie Zhu, Xueqiong |
author_facet | Wang, Han Chen, Xin Jin, Yanshan Liu, Tingxian Song, Yizuo Zhu, Xuejie Zhu, Xueqiong |
author_sort | Wang, Han |
collection | PubMed |
description | PURPOSE: DYNLT3 is identified as an age‐related gene. Nevertheless, the specific mechanism of its carcinogenesis in breast tumor has not been clarified. This research aims to elucidate the role and the underlying molecular pathways of DYNLT3 on breast cancer tumorigenesis. METHODS: The differential expression of DYNLT3 among breast cancer, breast fibroids, and normal tissues, as well as in various breast cancer cell lines were detected by immunohistochemical staining, real‐time quantitative reverse transcription‐PCR and Western blotting, respectively. Additionally, the role of DYNLT3 on cell viability and proliferation were observed through cell counting kit‐8, bromodeoxyuridine, and colony formation experiments. Migratory and invasive abilities was envaulted by wound healing and Transwell methods. Apoptotic cells rate was examined by flow cytometry. Furthermore, nude mice xenograft models were established to confirm the role of DYNLT3 in tumor formation in vivo. RESULTS: DYNLT3 expression was highly rising in both breast cancer tissues and cells. DYNLT3 knockdown obviously suppressed cell growth, migration and invasion, and induced cell apoptosis in MDA‐MB‐231 and MCF‐7 breast cancer cells. The overexpression of DYNLT3 exerted the opposite effect in MDA‐MB‐231 cells. Moreover, DYNLT3 knockdown inhibited tumor formation in vivo. Mechanistically, an elevation of N‐cadherin and vimentin levels and a decline of E‐cadherin were observed when DYNLT3 was upregulated, which was reversed when DYNLT3 knockdown was performed. CONCLUSION: DYNLT3 may function as a tumor‐promotor of age‐associated breast cancer, which is expected to provide experimental basis for new treatment options. |
format | Online Article Text |
id | pubmed-10417059 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-104170592023-08-12 The role of DYNLT3 in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition Wang, Han Chen, Xin Jin, Yanshan Liu, Tingxian Song, Yizuo Zhu, Xuejie Zhu, Xueqiong Cancer Med RESEARCH ARTICLES PURPOSE: DYNLT3 is identified as an age‐related gene. Nevertheless, the specific mechanism of its carcinogenesis in breast tumor has not been clarified. This research aims to elucidate the role and the underlying molecular pathways of DYNLT3 on breast cancer tumorigenesis. METHODS: The differential expression of DYNLT3 among breast cancer, breast fibroids, and normal tissues, as well as in various breast cancer cell lines were detected by immunohistochemical staining, real‐time quantitative reverse transcription‐PCR and Western blotting, respectively. Additionally, the role of DYNLT3 on cell viability and proliferation were observed through cell counting kit‐8, bromodeoxyuridine, and colony formation experiments. Migratory and invasive abilities was envaulted by wound healing and Transwell methods. Apoptotic cells rate was examined by flow cytometry. Furthermore, nude mice xenograft models were established to confirm the role of DYNLT3 in tumor formation in vivo. RESULTS: DYNLT3 expression was highly rising in both breast cancer tissues and cells. DYNLT3 knockdown obviously suppressed cell growth, migration and invasion, and induced cell apoptosis in MDA‐MB‐231 and MCF‐7 breast cancer cells. The overexpression of DYNLT3 exerted the opposite effect in MDA‐MB‐231 cells. Moreover, DYNLT3 knockdown inhibited tumor formation in vivo. Mechanistically, an elevation of N‐cadherin and vimentin levels and a decline of E‐cadherin were observed when DYNLT3 was upregulated, which was reversed when DYNLT3 knockdown was performed. CONCLUSION: DYNLT3 may function as a tumor‐promotor of age‐associated breast cancer, which is expected to provide experimental basis for new treatment options. John Wiley and Sons Inc. 2023-06-01 /pmc/articles/PMC10417059/ /pubmed/37260179 http://dx.doi.org/10.1002/cam4.6173 Text en © 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | RESEARCH ARTICLES Wang, Han Chen, Xin Jin, Yanshan Liu, Tingxian Song, Yizuo Zhu, Xuejie Zhu, Xueqiong The role of DYNLT3 in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition |
title | The role of
DYNLT3
in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition |
title_full | The role of
DYNLT3
in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition |
title_fullStr | The role of
DYNLT3
in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition |
title_full_unstemmed | The role of
DYNLT3
in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition |
title_short | The role of
DYNLT3
in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition |
title_sort | role of
dynlt3
in breast cancer proliferation, migration, and invasion via epithelial‐to‐mesenchymal transition |
topic | RESEARCH ARTICLES |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10417059/ https://www.ncbi.nlm.nih.gov/pubmed/37260179 http://dx.doi.org/10.1002/cam4.6173 |
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