Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway

DNA damage plays a key role in various biological processes involved in malignant disease, the role of the DNA damage repair gene EME1 (essential meiotic structure-specific endonuclease 1) in gastric cancer (GC) development is unknown. This work aimed to investigate expression and role of EME1 in tu...

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Autores principales: Zhiguo Guo, Erbo Liang, Wei Li, Leilei Jiang, Fachao Zhi
Formato: article
Lenguaje:EN
Publicado: Taylor & Francis Group 2021
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Acceso en línea:https://doaj.org/article/49e43532a4754895868057142feb7588
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spelling oai:doaj.org-article:49e43532a4754895868057142feb75882021-11-04T15:51:54ZEssential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway2165-59792165-598710.1080/21655979.2021.1999371https://doaj.org/article/49e43532a4754895868057142feb75882021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1999371https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987DNA damage plays a key role in various biological processes involved in malignant disease, the role of the DNA damage repair gene EME1 (essential meiotic structure-specific endonuclease 1) in gastric cancer (GC) development is unknown. This work aimed to investigate expression and role of EME1 in tumorigenesis. Quantitative real-time polymerase chain reaction (qRT-PCR), immunoblot, cell viability and dual-luciferase reporter assays, RNAi and gene transfection, and immunofluorescent staining were performed to assess EME1 regulation in GC tumorigenesis. Further, mouse xenografts were established for in vivo mechanistic studies. EME1 was found to be upregulated in both gastric cancer cells and clinically obtained tumors. Additionally, EME1 levels were strongly associated with the differentiation level of GC and lymph node metastasis. In vivo and in vitro knockdown of EME1 markedly suppressed the proliferative, migratory, and invasive abilities of GC cells and enhanced apoptotic cell death and cell cycle arrest rates. Mechanistically, EME1 modulated Akt/GSK3B/CCND1 signaling. MYB may also have contributed to EME1-dependent gastric carcinogenesis. Elevated EME1 expressions may enhance the proliferative and metastatic abilities of GC cells, thereby acting as a tumor-promoting factor via Akt. These findings reveal that EME1 is an important biomarker for GC prognosis and treatment in humans.Zhiguo GuoErbo LiangWei LiLeilei JiangFachao ZhiTaylor & Francis Grouparticleeme1gastric cancerakt/gsk3b/ccnd1proliferationinvasionBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution DOAJ
collection DOAJ
language EN
topic eme1
gastric cancer
akt/gsk3b/ccnd1
proliferation
invasion
Biotechnology
TP248.13-248.65
spellingShingle eme1
gastric cancer
akt/gsk3b/ccnd1
proliferation
invasion
Biotechnology
TP248.13-248.65
Zhiguo Guo
Erbo Liang
Wei Li
Leilei Jiang
Fachao Zhi
Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway
description DNA damage plays a key role in various biological processes involved in malignant disease, the role of the DNA damage repair gene EME1 (essential meiotic structure-specific endonuclease 1) in gastric cancer (GC) development is unknown. This work aimed to investigate expression and role of EME1 in tumorigenesis. Quantitative real-time polymerase chain reaction (qRT-PCR), immunoblot, cell viability and dual-luciferase reporter assays, RNAi and gene transfection, and immunofluorescent staining were performed to assess EME1 regulation in GC tumorigenesis. Further, mouse xenografts were established for in vivo mechanistic studies. EME1 was found to be upregulated in both gastric cancer cells and clinically obtained tumors. Additionally, EME1 levels were strongly associated with the differentiation level of GC and lymph node metastasis. In vivo and in vitro knockdown of EME1 markedly suppressed the proliferative, migratory, and invasive abilities of GC cells and enhanced apoptotic cell death and cell cycle arrest rates. Mechanistically, EME1 modulated Akt/GSK3B/CCND1 signaling. MYB may also have contributed to EME1-dependent gastric carcinogenesis. Elevated EME1 expressions may enhance the proliferative and metastatic abilities of GC cells, thereby acting as a tumor-promoting factor via Akt. These findings reveal that EME1 is an important biomarker for GC prognosis and treatment in humans.
format article
author Zhiguo Guo
Erbo Liang
Wei Li
Leilei Jiang
Fachao Zhi
author_facet Zhiguo Guo
Erbo Liang
Wei Li
Leilei Jiang
Fachao Zhi
author_sort Zhiguo Guo
title Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway
title_short Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway
title_full Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway
title_fullStr Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway
title_full_unstemmed Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway
title_sort essential meiotic structure-specific endonuclease1 (eme1) promotes malignant features in gastric cancer cells via the akt/gsk3b/ccnd1 pathway
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/49e43532a4754895868057142feb7588
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