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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Taylor & Francis Group
2021
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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) |
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eme1 gastric cancer akt/gsk3b/ccnd1 proliferation invasion Biotechnology TP248.13-248.65 |
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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 |
work_keys_str_mv |
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