PMID- 33416213
OWN - NLM
STAT- MEDLINE
DCOM- 20211115
LR  - 20211115
IS  - 2056-4538 (Electronic)
IS  - 2056-4538 (Linking)
VI  - 7
IP  - 2
DP  - 2021 Mar
TI  - PRMT5 promotes progression of endometrioid adenocarcinoma via ERalpha and cell cycle 
      signaling pathways.
PG  - 154-164
LID - 10.1002/cjp2.194 [doi]
AB  - 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 alpha (ERalpha), and related functional proteins. Coimmunoprecipitation 
      was performed to examine the interaction of PRMT5 with ERalpha 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 ERalpha and SRC1 to promote the expression of ERalpha. In conclusion, PRMT5 plays a 
      significant role in the progression of EAC by interacting with ERalpha and impacting 
      the cell cycle signaling pathways.
CI  - (c) 2021 The Authors. The Journal of Pathology: Clinical Research published by The 
      Pathological Society of Great Britain and Ireland & John Wiley & Sons, Ltd.
FAU - Mei, Shuyu
AU  - Mei S
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
AD  - Department of Pathology, Bao Di Hospital, Bao Di Clinical College of Tianjin 
      Medical University, Tianjin, PR China.
FAU - Ge, Shuang
AU  - Ge S
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
FAU - Wang, Jun
AU  - Wang J
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
FAU - Li, Hailing
AU  - Li H
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
FAU - Jing, Xiaotong
AU  - Jing X
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
FAU - Liang, Ke
AU  - Liang K
AD  - Department of Pathology, Qilu Hospital of Shandong University, Jinan, PR China.
FAU - Zhang, Xiaoying
AU  - Zhang X
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
FAU - Xue, Chaoshuai
AU  - Xue C
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
FAU - Zhang, Cuijuan
AU  - Zhang C
AUID- ORCID: 0000-0002-1268-9349
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
AD  - Department of Pathology, Qilu Hospital of Shandong University, Jinan, PR China.
FAU - Zhang, Tingguo
AU  - Zhang T
AD  - Institute of Pathology and Pathophysiology, Shandong University School of 
      Medicine, Jinan, PR China.
AD  - Department of Pathology, Qilu Hospital of Shandong University, Jinan, PR China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210108
PL  - England
TA  - J Pathol Clin Res
JT  - The journal of pathology. Clinical research
JID - 101658534
RN  - 0 (ESR1 protein, human)
RN  - 0 (Estrogen Receptor alpha)
RN  - EC 2.1.1.319 (PRMT5 protein, human)
RN  - EC 2.1.1.319 (Protein-Arginine N-Methyltransferases)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Apoptosis
MH  - Carcinogenesis
MH  - Carcinoma, Endometrioid/*genetics/metabolism/pathology
MH  - Cell Cycle
MH  - Cell Line, Tumor
MH  - Endometrial Neoplasms/*genetics/metabolism/pathology
MH  - Estrogen Receptor alpha/genetics/*metabolism
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Immunohistochemistry
MH  - Middle Aged
MH  - Protein-Arginine N-Methyltransferases/genetics/*metabolism
MH  - *Signal Transduction
MH  - Up-Regulation
PMC - PMC7869932
OTO - NOTNLM
OT  - ERalpha
OT  - PRMT5
OT  - cell function
OT  - endometrial cancer
OT  - epigenetics
EDAT- 2021/01/09 06:00
MHDA- 2021/11/16 06:00
PMCR- 2021/01/08
CRDT- 2021/01/08 08:37
PHST- 2020/08/01 00:00 [received]
PHST- 2020/11/15 00:00 [revised]
PHST- 2020/11/18 00:00 [accepted]
PHST- 2021/01/09 06:00 [pubmed]
PHST- 2021/11/16 06:00 [medline]
PHST- 2021/01/08 08:37 [entrez]
PHST- 2021/01/08 00:00 [pmc-release]
AID - CJP2194 [pii]
AID - 10.1002/cjp2.194 [doi]
PST - ppublish
SO  - J Pathol Clin Res. 2021 Mar;7(2):154-164. doi: 10.1002/cjp2.194. Epub 2021 Jan 8.