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Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival

AIM: In our previous report, we identified roles of CLDN7 in regulation of cell signaling. The goal of this study was to identify proteins interacting with CLDN7 in ovarian cancer. METHODS: The yeast two-hybrid system was used to identify proteins directly interacting with CLDN7 and cell survival wa...

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Autor principal: Dahiya, Neetu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Future Science Ltd 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7117550/
https://www.ncbi.nlm.nih.gov/pubmed/32257370
http://dx.doi.org/10.2144/fsoa-2019-0123
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author Dahiya, Neetu
author_facet Dahiya, Neetu
author_sort Dahiya, Neetu
collection PubMed
description AIM: In our previous report, we identified roles of CLDN7 in regulation of cell signaling. The goal of this study was to identify proteins interacting with CLDN7 in ovarian cancer. METHODS: The yeast two-hybrid system was used to identify proteins directly interacting with CLDN7 and cell survival was tested using colony formation assay. RESULTS: Amyloid precursor-like protein 2 (APLP2) was found directly associated with CLDN7 in ovarian cancer cell line OVCA420. In addition, APLP2 showed increased expression in ovarian cancer cell lines and tumor tissue samples compared with non-neoplastic ovarian tissues. Knockdown of CLDN7 led to increased expression of APLP2 at both the mRNA and protein levels. Knockdown of APLP2 was associated with decreased cell survival in ovarian cancer cells. CONCLUSION: We show a direct interaction of CLDN7 with APLP2. These findings suggest novel regulatory role for APLP2 in ovarian cancer, a role that appears to be mediated by CLDN7.
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spelling pubmed-71175502020-04-06 Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival Dahiya, Neetu Future Sci OA Research Article AIM: In our previous report, we identified roles of CLDN7 in regulation of cell signaling. The goal of this study was to identify proteins interacting with CLDN7 in ovarian cancer. METHODS: The yeast two-hybrid system was used to identify proteins directly interacting with CLDN7 and cell survival was tested using colony formation assay. RESULTS: Amyloid precursor-like protein 2 (APLP2) was found directly associated with CLDN7 in ovarian cancer cell line OVCA420. In addition, APLP2 showed increased expression in ovarian cancer cell lines and tumor tissue samples compared with non-neoplastic ovarian tissues. Knockdown of CLDN7 led to increased expression of APLP2 at both the mRNA and protein levels. Knockdown of APLP2 was associated with decreased cell survival in ovarian cancer cells. CONCLUSION: We show a direct interaction of CLDN7 with APLP2. These findings suggest novel regulatory role for APLP2 in ovarian cancer, a role that appears to be mediated by CLDN7. Future Science Ltd 2020-03-16 /pmc/articles/PMC7117550/ /pubmed/32257370 http://dx.doi.org/10.2144/fsoa-2019-0123 Text en © 2020 NIH This work is licensed under the Creative Commons Attribution 4.0 License (http://creativecommons.org/licenses/by/4.0/)
spellingShingle Research Article
Dahiya, Neetu
Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival
title Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival
title_full Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival
title_fullStr Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival
title_full_unstemmed Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival
title_short Amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival
title_sort amyloid precursor-like protein 2 interacts with claudin-7 and affects ovarian cancer cell survival
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7117550/
https://www.ncbi.nlm.nih.gov/pubmed/32257370
http://dx.doi.org/10.2144/fsoa-2019-0123
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