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FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16
Lung cancer is a common type of cancer that represents a health problem worldwide; lung adenocarcinoma (LUAD) is a major subtype of lung cancer. Although several treatments for LUAD have been developed, the mortality rate remains high because of uncontrollable progression. Further biological and cli...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7385341/ https://www.ncbi.nlm.nih.gov/pubmed/32418298 http://dx.doi.org/10.1111/cas.14483 |
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author | Kawasaki, Keisuke Nojima, Satoshi Hijiki, Sachiko Tahara, Shinichiro Ohshima, Kenji Matsui, Takahiro Hori, Yumiko Kurashige, Masako Umeda, Daisuke Kiyokawa, Hiroki Kido, Kansuke Okuzaki, Daisuke Morii, Eiichi |
author_facet | Kawasaki, Keisuke Nojima, Satoshi Hijiki, Sachiko Tahara, Shinichiro Ohshima, Kenji Matsui, Takahiro Hori, Yumiko Kurashige, Masako Umeda, Daisuke Kiyokawa, Hiroki Kido, Kansuke Okuzaki, Daisuke Morii, Eiichi |
author_sort | Kawasaki, Keisuke |
collection | PubMed |
description | Lung cancer is a common type of cancer that represents a health problem worldwide; lung adenocarcinoma (LUAD) is a major subtype of lung cancer. Although several treatments for LUAD have been developed, the mortality rate remains high because of uncontrollable progression. Further biological and clinicopathological studies are therefore needed. Here, we investigated the role of family with sequence similarity 111 member B (FAM111B), which is highly expressed in papillary‐predominant LUAD; however, its role in cancer is unclear. An immunohistochemical analysis confirmed that papillary‐predominant adenocarcinomas exhibited higher expression of FAM111B, compared with lepidic‐predominant adenocarcinomas. Additionally, FAM111B expression was significantly correlated with clinical progression. In vitro functional analyses using FAM111B‐knockout cells demonstrated that FAM111B plays an important role in proliferation and cell cycle progression of KRAS‐driven LUAD under serum‐starvation conditions. Furthermore, FAM111B regulated cyclin D1‐CDK4‐dependent cell cycle progression by degradation of p16. In summary, we revealed the clinical importance of FAM111B in human tumor tissues, as well as its function as a degradative enzyme. Therefore, FAM111B has potential as a clinicopathological prognostic marker for LUAD. |
format | Online Article Text |
id | pubmed-7385341 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73853412020-07-30 FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16 Kawasaki, Keisuke Nojima, Satoshi Hijiki, Sachiko Tahara, Shinichiro Ohshima, Kenji Matsui, Takahiro Hori, Yumiko Kurashige, Masako Umeda, Daisuke Kiyokawa, Hiroki Kido, Kansuke Okuzaki, Daisuke Morii, Eiichi Cancer Sci Original Articles Lung cancer is a common type of cancer that represents a health problem worldwide; lung adenocarcinoma (LUAD) is a major subtype of lung cancer. Although several treatments for LUAD have been developed, the mortality rate remains high because of uncontrollable progression. Further biological and clinicopathological studies are therefore needed. Here, we investigated the role of family with sequence similarity 111 member B (FAM111B), which is highly expressed in papillary‐predominant LUAD; however, its role in cancer is unclear. An immunohistochemical analysis confirmed that papillary‐predominant adenocarcinomas exhibited higher expression of FAM111B, compared with lepidic‐predominant adenocarcinomas. Additionally, FAM111B expression was significantly correlated with clinical progression. In vitro functional analyses using FAM111B‐knockout cells demonstrated that FAM111B plays an important role in proliferation and cell cycle progression of KRAS‐driven LUAD under serum‐starvation conditions. Furthermore, FAM111B regulated cyclin D1‐CDK4‐dependent cell cycle progression by degradation of p16. In summary, we revealed the clinical importance of FAM111B in human tumor tissues, as well as its function as a degradative enzyme. Therefore, FAM111B has potential as a clinicopathological prognostic marker for LUAD. John Wiley and Sons Inc. 2020-06-03 2020-07 /pmc/articles/PMC7385341/ /pubmed/32418298 http://dx.doi.org/10.1111/cas.14483 Text en © 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Articles Kawasaki, Keisuke Nojima, Satoshi Hijiki, Sachiko Tahara, Shinichiro Ohshima, Kenji Matsui, Takahiro Hori, Yumiko Kurashige, Masako Umeda, Daisuke Kiyokawa, Hiroki Kido, Kansuke Okuzaki, Daisuke Morii, Eiichi FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16 |
title | FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16 |
title_full | FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16 |
title_fullStr | FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16 |
title_full_unstemmed | FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16 |
title_short | FAM111B enhances proliferation of KRAS‐driven lung adenocarcinoma by degrading p16 |
title_sort | fam111b enhances proliferation of kras‐driven lung adenocarcinoma by degrading p16 |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7385341/ https://www.ncbi.nlm.nih.gov/pubmed/32418298 http://dx.doi.org/10.1111/cas.14483 |
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