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LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway

BACKGROUND: LNK adaptor protein is a crucial regulator of normal hematopoiesis, which down-regulates activated tyrosine kinases at the cell surface resulting in an antitumor effect. To date, little studies have examined activities of LNK in solid tumors except ovarian cancer. METHODS: Clinical tissu...

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Autores principales: Lv, Jianxin, Yu, Wei, Zhang, Yanan, Cao, Xinhua, Han, Lifei, Hu, Haolin, Wang, Chenfei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7160949/
https://www.ncbi.nlm.nih.gov/pubmed/32322171
http://dx.doi.org/10.1186/s12935-020-01197-9
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author Lv, Jianxin
Yu, Wei
Zhang, Yanan
Cao, Xinhua
Han, Lifei
Hu, Haolin
Wang, Chenfei
author_facet Lv, Jianxin
Yu, Wei
Zhang, Yanan
Cao, Xinhua
Han, Lifei
Hu, Haolin
Wang, Chenfei
author_sort Lv, Jianxin
collection PubMed
description BACKGROUND: LNK adaptor protein is a crucial regulator of normal hematopoiesis, which down-regulates activated tyrosine kinases at the cell surface resulting in an antitumor effect. To date, little studies have examined activities of LNK in solid tumors except ovarian cancer. METHODS: Clinical tissue chips were obtained from 16 clinical patients after surgery. Western blotting assay and quantitative real time PCR was performed to measure the expression of LNK. We investigate the in vivo and vitro effect of LNK in Triple Negative Breast Cancer by using cell proliferation、migration assays and an in vivo murine xenograft model. Western blotting assay was performed to investigate the mechanism of LNK in triple negative breast cancer. RESULTS: We found that the levels of LNK expression were elevated in high grade triple-negative breast cancer through Clinical tissue chips. Remarkably, overexpression of LNK can promote breast cancer cell proliferation and migration in vivo and vitro, while silencing of LNK show the opposite phenomenon. We also found that LNK can promote breast cancer cell to proliferate and migrate via activating JAK/STAT3 and ERK1/2 pathway. CONCLUSIONS: Our results suggest that the adaptor protein LNK acts as a positive signal transduction modulator in TNBC.
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spelling pubmed-71609492020-04-22 LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway Lv, Jianxin Yu, Wei Zhang, Yanan Cao, Xinhua Han, Lifei Hu, Haolin Wang, Chenfei Cancer Cell Int Primary Research BACKGROUND: LNK adaptor protein is a crucial regulator of normal hematopoiesis, which down-regulates activated tyrosine kinases at the cell surface resulting in an antitumor effect. To date, little studies have examined activities of LNK in solid tumors except ovarian cancer. METHODS: Clinical tissue chips were obtained from 16 clinical patients after surgery. Western blotting assay and quantitative real time PCR was performed to measure the expression of LNK. We investigate the in vivo and vitro effect of LNK in Triple Negative Breast Cancer by using cell proliferation、migration assays and an in vivo murine xenograft model. Western blotting assay was performed to investigate the mechanism of LNK in triple negative breast cancer. RESULTS: We found that the levels of LNK expression were elevated in high grade triple-negative breast cancer through Clinical tissue chips. Remarkably, overexpression of LNK can promote breast cancer cell proliferation and migration in vivo and vitro, while silencing of LNK show the opposite phenomenon. We also found that LNK can promote breast cancer cell to proliferate and migrate via activating JAK/STAT3 and ERK1/2 pathway. CONCLUSIONS: Our results suggest that the adaptor protein LNK acts as a positive signal transduction modulator in TNBC. BioMed Central 2020-04-15 /pmc/articles/PMC7160949/ /pubmed/32322171 http://dx.doi.org/10.1186/s12935-020-01197-9 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.
spellingShingle Primary Research
Lv, Jianxin
Yu, Wei
Zhang, Yanan
Cao, Xinhua
Han, Lifei
Hu, Haolin
Wang, Chenfei
LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway
title LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway
title_full LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway
title_fullStr LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway
title_full_unstemmed LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway
title_short LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway
title_sort lnk promotes the growth and metastasis of triple negative breast cancer via activating jak/stat3 and erk1/2 pathway
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7160949/
https://www.ncbi.nlm.nih.gov/pubmed/32322171
http://dx.doi.org/10.1186/s12935-020-01197-9
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