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AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression
AIM: To investigate whether AF1q, overexpressed in metastatic cells compared with the primary tumor cells, plays a pivotal role in breast cancer metastasis. METHODS: To investigate whether AF1q has a responsibility in the acquisition of a metastatic phenotype, we performed RNA-sequencing (RNA-Seq) t...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6623974/ https://www.ncbi.nlm.nih.gov/pubmed/31297450 http://dx.doi.org/10.20517/2394-4722.2018.84 |
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author | Park, Jino Hwang, Jae Yeon Thore, Alexandra Kim, Soojin Togano, Tomiteru Hagiwara, Shotaro Park, Juw Won Tse, William |
author_facet | Park, Jino Hwang, Jae Yeon Thore, Alexandra Kim, Soojin Togano, Tomiteru Hagiwara, Shotaro Park, Juw Won Tse, William |
author_sort | Park, Jino |
collection | PubMed |
description | AIM: To investigate whether AF1q, overexpressed in metastatic cells compared with the primary tumor cells, plays a pivotal role in breast cancer metastasis. METHODS: To investigate whether AF1q has a responsibility in the acquisition of a metastatic phenotype, we performed RNA-sequencing (RNA-Seq) to identify the gene signature and applied the Metacore direct interactions network building algorithm with the top 40 amplicons of RNA-Seq. RESULTS: Most genes were directly linked with intercellular adhesion molecule-1 (ICAM-1). Likewise, we identified that ICAM-1 expression is attenuated in metastatic cells compared to primary tumor cells. Moreover, overexpression of AF1q attenuated ICAM-1 expression, whereas suppression of AF1q elicited the opposite effect. AF1q had an effect on ICAM-1 promoter region and regulated its transcription. Decreased ICAM-1 expression affected the attachment of T cells to a breast cancer cell monolayer. We confirmed the finding by performing the analysis on Burkitt’s lymphoma. CONCLUSION: Attenuation of ICAM-1 by AF1q on tumor cells disadvantages host anti-tumor defenses through the trafficking of lymphocytes, which affects tumor progression and metastasis. |
format | Online Article Text |
id | pubmed-6623974 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
record_format | MEDLINE/PubMed |
spelling | pubmed-66239742019-07-11 AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression Park, Jino Hwang, Jae Yeon Thore, Alexandra Kim, Soojin Togano, Tomiteru Hagiwara, Shotaro Park, Juw Won Tse, William J Cancer Metastasis Treat Article AIM: To investigate whether AF1q, overexpressed in metastatic cells compared with the primary tumor cells, plays a pivotal role in breast cancer metastasis. METHODS: To investigate whether AF1q has a responsibility in the acquisition of a metastatic phenotype, we performed RNA-sequencing (RNA-Seq) to identify the gene signature and applied the Metacore direct interactions network building algorithm with the top 40 amplicons of RNA-Seq. RESULTS: Most genes were directly linked with intercellular adhesion molecule-1 (ICAM-1). Likewise, we identified that ICAM-1 expression is attenuated in metastatic cells compared to primary tumor cells. Moreover, overexpression of AF1q attenuated ICAM-1 expression, whereas suppression of AF1q elicited the opposite effect. AF1q had an effect on ICAM-1 promoter region and regulated its transcription. Decreased ICAM-1 expression affected the attachment of T cells to a breast cancer cell monolayer. We confirmed the finding by performing the analysis on Burkitt’s lymphoma. CONCLUSION: Attenuation of ICAM-1 by AF1q on tumor cells disadvantages host anti-tumor defenses through the trafficking of lymphocytes, which affects tumor progression and metastasis. 2019-03-18 2019 /pmc/articles/PMC6623974/ /pubmed/31297450 http://dx.doi.org/10.20517/2394-4722.2018.84 Text en This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as 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. |
spellingShingle | Article Park, Jino Hwang, Jae Yeon Thore, Alexandra Kim, Soojin Togano, Tomiteru Hagiwara, Shotaro Park, Juw Won Tse, William AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression |
title | AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression |
title_full | AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression |
title_fullStr | AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression |
title_full_unstemmed | AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression |
title_short | AF1q inhibited T cell attachment to breast cancer cell by attenuating Intracellular Adhesion Molecule-1 expression |
title_sort | af1q inhibited t cell attachment to breast cancer cell by attenuating intracellular adhesion molecule-1 expression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6623974/ https://www.ncbi.nlm.nih.gov/pubmed/31297450 http://dx.doi.org/10.20517/2394-4722.2018.84 |
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