PMID- 35613689
OWN - NLM
STAT- MEDLINE
DCOM- 20220614
LR  - 20220630
IS  - 1096-0384 (Electronic)
IS  - 0003-9861 (Linking)
VI  - 725
DP  - 2022 Aug 15
TI  - ESR1 inhibits ionizing radiation-induced ferroptosis in breast cancer cells via 
      the NEDD4L/CD71 pathway.
PG  - 109299
LID - S0003-9861(22)00183-7 [pii]
LID - 10.1016/j.abb.2022.109299 [doi]
AB  - Ferroptosis is the name given to the type of non-apoptotic cell death that is 
      caused by iron accumulation and subsequent lipid peroxidation. However, how 
      ionizing radiation (IR)-induced ferroptosis is regulated in estrogen 
      receptor-positive (ER(+)) breast cancer cells remains unclear. To attempt to 
      resolve this issue, bioinformatics analysis was performed to evaluate the 
      prognostic value of estrogen receptor 1 (ESR1) in breast cancer tissues. A total 
      of four breast cancer cell lines and an MCF10A non-malignant counterpart were 
      used. Western blotting was used to analyze the levels of protein expression, 
      whereas immunoprecipitation (IP) and ubiquitination experiments were used to test 
      protein binding and ubiquitination levels, respectively. Flow cytometry was 
      subsequently used to analyze cell death and lipid peroxidation levels. The 
      results showed that a high expression level of ESR1 was significantly correlated 
      with poor overall survival in breast cancer. ESR1 knockdown significantly 
      enhanced IR-induced ferroptosis and increased the CD71 protein level. The IP 
      results showed that ESR1 enhanced the binding of the E3 ubiquitin ligase NEDD4L 
      to CD71, promoting the ubiquitination and degradation of CD71, suggesting that 
      CD71 expression was regulated by both ESR1 and NEDD4L. Taken together, the 
      findings in the present study have demonstrated a regulatory relationship between 
      ESR1 and NEDD4L/CD71 in IR-induced ferroptosis. In addition, the ESR1/NEDD4L/CD71 
      axis may be a potential target for the radiotherapy of breast cancer.
CI  - Copyright (c) 2022 Elsevier Inc. All rights reserved.
FAU - Liu, Lin
AU  - Liu L
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China.
FAU - Zhang, Chen
AU  - Zhang C
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China.
FAU - Qu, Shugen
AU  - Qu S
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China.
FAU - Liu, Rui
AU  - Liu R
AD  - NHC Key Laboratory of Radiobiology, School of Public Health of Jilin University, 
      Changchun, Jilin, 130021, China.
FAU - Chen, Huajian
AU  - Chen H
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China.
FAU - Liang, Zhenzhen
AU  - Liang Z
AD  - NHC Key Laboratory of Radiobiology, School of Public Health of Jilin University, 
      Changchun, Jilin, 130021, China.
FAU - Tian, Zhujun
AU  - Tian Z
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China.
FAU - Li, Lan
AU  - Li L
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China.
FAU - Ma, Shumei
AU  - Ma S
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China; Key Laboratory of Watershed Science and Health of 
      Zhejiang Province, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China; 
      South Zhejiang Institute of Radiation Medicine and Nuclear Technology, Wenzhou, 
      Zhejiang, 325035, China. Electronic address: shmm2001@126.com.
FAU - Liu, Xiaodong
AU  - Liu X
AD  - School of Public Health and Management, Wenzhou Medical University, Wenzhou, 
      Zhejiang, 325035, China; Key Laboratory of Watershed Science and Health of 
      Zhejiang Province, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China. 
      Electronic address: liuxd2014@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220522
PL  - United States
TA  - Arch Biochem Biophys
JT  - Archives of biochemistry and biophysics
JID - 0372430
RN  - 0 (Antigens, CD)
RN  - 0 (CD71 antigen)
RN  - 0 (ESR1 protein, human)
RN  - 0 (Estrogen Receptor alpha)
RN  - 0 (Receptors, Transferrin)
RN  - EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases)
RN  - EC 2.3.2.26 (Nedd4L protein, human)
SB  - IM
MH  - Antigens, CD/metabolism
MH  - *Breast Neoplasms/genetics/metabolism/radiotherapy
MH  - Estrogen Receptor alpha/genetics/*metabolism
MH  - Female
MH  - *Ferroptosis
MH  - Humans
MH  - MCF-7 Cells
MH  - Nedd4 Ubiquitin Protein Ligases/metabolism
MH  - Radiation, Ionizing
MH  - Receptors, Transferrin/metabolism
OTO - NOTNLM
OT  - Breast cancer
OT  - Estrogen receptor 1
OT  - Ferroptosis
OT  - Ionizing radiation
OT  - NEDD4L
OT  - Transferrin receptor (CD71)
EDAT- 2022/05/26 06:00
MHDA- 2022/06/15 06:00
CRDT- 2022/05/25 19:24
PHST- 2022/03/20 00:00 [received]
PHST- 2022/05/18 00:00 [revised]
PHST- 2022/05/19 00:00 [accepted]
PHST- 2022/05/26 06:00 [pubmed]
PHST- 2022/06/15 06:00 [medline]
PHST- 2022/05/25 19:24 [entrez]
AID - S0003-9861(22)00183-7 [pii]
AID - 10.1016/j.abb.2022.109299 [doi]
PST - ppublish
SO  - Arch Biochem Biophys. 2022 Aug 15;725:109299. doi: 10.1016/j.abb.2022.109299. 
      Epub 2022 May 22.