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PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways

Protein arginine methyltransferase 5 (PRMT5) has previously been reported to be upregulated in many malignant tumors. This study investigated the significance of PRMT5 in endometrial carcinoma (EC) and explored its function in tumorigenesis. Immunohistochemistry was performed to evaluate PRMT5 expre...

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Autores principales: Mei, Shuyu, Ge, Shuang, Wang, Jun, Li, Hailing, Jing, Xiaotong, Liang, Ke, Zhang, Xiaoying, Xue, Chaoshuai, Zhang, Cuijuan, Zhang, Tingguo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7869932/
https://www.ncbi.nlm.nih.gov/pubmed/33416213
http://dx.doi.org/10.1002/cjp2.194
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author Mei, Shuyu
Ge, Shuang
Wang, Jun
Li, Hailing
Jing, Xiaotong
Liang, Ke
Zhang, Xiaoying
Xue, Chaoshuai
Zhang, Cuijuan
Zhang, Tingguo
author_facet Mei, Shuyu
Ge, Shuang
Wang, Jun
Li, Hailing
Jing, Xiaotong
Liang, Ke
Zhang, Xiaoying
Xue, Chaoshuai
Zhang, Cuijuan
Zhang, Tingguo
author_sort Mei, Shuyu
collection PubMed
description Protein arginine methyltransferase 5 (PRMT5) has previously been reported to be upregulated in many malignant tumors. This study investigated the significance of PRMT5 in endometrial carcinoma (EC) and explored its function in tumorigenesis. Immunohistochemistry was performed to evaluate PRMT5 expression in 62 EC and 66 endometrial hyperplasia samples. The functions of PRMT5 were investigated by cell counting kit‐8, plate colony formation, wound healing, and transwell and flow cytometry assays. Quantitative reverse transcription‐polymerase chain reaction and western blotting were used to measure the expression of PRMT5, changes in estrogen receptor α (ERα), and related functional proteins. Coimmunoprecipitation was performed to examine the interaction of PRMT5 with ERα and its coactivator steroid receptor coactivator‐1 (SRC1). Compared to endometrial hyperplasia tissue, PRMT5 was overexpressed in endometrioid adenocarcinoma (EAC) but not overexpressed in mucinous EC. The main expression pattern of PRMT5 in EAC was cytoplasmic. However, the positive cases of endometrial hyperplasia showed both cytoplasmic and nuclear positivity in the endometrial glands or were mainly positive in stromal cells. Knockdown of PRMT5 significantly inhibited the growth and migration ability of EAC cells and promoted their apoptosis by regulating cyclin D1, c‐myc, p53, and Bcl2 proteins. Furthermore, PRMT5 could form a complex with ERα and SRC1 to promote the expression of ERα. In conclusion, PRMT5 plays a significant role in the progression of EAC by interacting with ERα and impacting the cell cycle signaling pathways.
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spelling pubmed-78699322021-02-17 PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways Mei, Shuyu Ge, Shuang Wang, Jun Li, Hailing Jing, Xiaotong Liang, Ke Zhang, Xiaoying Xue, Chaoshuai Zhang, Cuijuan Zhang, Tingguo J Pathol Clin Res Original Articles Protein arginine methyltransferase 5 (PRMT5) has previously been reported to be upregulated in many malignant tumors. This study investigated the significance of PRMT5 in endometrial carcinoma (EC) and explored its function in tumorigenesis. Immunohistochemistry was performed to evaluate PRMT5 expression in 62 EC and 66 endometrial hyperplasia samples. The functions of PRMT5 were investigated by cell counting kit‐8, plate colony formation, wound healing, and transwell and flow cytometry assays. Quantitative reverse transcription‐polymerase chain reaction and western blotting were used to measure the expression of PRMT5, changes in estrogen receptor α (ERα), and related functional proteins. Coimmunoprecipitation was performed to examine the interaction of PRMT5 with ERα and its coactivator steroid receptor coactivator‐1 (SRC1). Compared to endometrial hyperplasia tissue, PRMT5 was overexpressed in endometrioid adenocarcinoma (EAC) but not overexpressed in mucinous EC. The main expression pattern of PRMT5 in EAC was cytoplasmic. However, the positive cases of endometrial hyperplasia showed both cytoplasmic and nuclear positivity in the endometrial glands or were mainly positive in stromal cells. Knockdown of PRMT5 significantly inhibited the growth and migration ability of EAC cells and promoted their apoptosis by regulating cyclin D1, c‐myc, p53, and Bcl2 proteins. Furthermore, PRMT5 could form a complex with ERα and SRC1 to promote the expression of ERα. In conclusion, PRMT5 plays a significant role in the progression of EAC by interacting with ERα and impacting the cell cycle signaling pathways. John Wiley & Sons, Inc. 2021-01-08 /pmc/articles/PMC7869932/ /pubmed/33416213 http://dx.doi.org/10.1002/cjp2.194 Text en © 2021 The Authors. The Journal of Pathology: Clinical Research published by The Pathological Society of Great Britain and Ireland & John Wiley & Sons, Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Mei, Shuyu
Ge, Shuang
Wang, Jun
Li, Hailing
Jing, Xiaotong
Liang, Ke
Zhang, Xiaoying
Xue, Chaoshuai
Zhang, Cuijuan
Zhang, Tingguo
PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways
title PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways
title_full PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways
title_fullStr PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways
title_full_unstemmed PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways
title_short PRMT5 promotes progression of endometrioid adenocarcinoma via ERα and cell cycle signaling pathways
title_sort prmt5 promotes progression of endometrioid adenocarcinoma via erα and cell cycle signaling pathways
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7869932/
https://www.ncbi.nlm.nih.gov/pubmed/33416213
http://dx.doi.org/10.1002/cjp2.194
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