PMID- 36544694
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20221223
IS  - 2305-5839 (Print)
IS  - 2305-5847 (Electronic)
IS  - 2305-5839 (Linking)
VI  - 10
IP  - 22
DP  - 2022 Nov
TI  - Isorhamnetin inhibits progression of ovarian cancer by targeting ESR1.
PG  - 1216
LID - 10.21037/atm-22-5064 [doi]
LID - 1216
AB  - BACKGROUND: Although reports suggest Chinese herbal medicine treatment of ovarian 
      cancer (OC) has a good effect, the role of isorhamnetin (ISO), a flavonol 
      aglycone with immune, anti-inflammatory, cardiovascular and cerebrovascular 
      protective effects, as well as an anticancer effect, in OC remains unclear. 
      Network pharmacology was used to explore this in vitro and in vivo, and to 
      identify relevant targets. METHODS: The common targets of ISO in the treatment of 
      OC were screened by constructing drug targets and disease gene databases for Gene 
      Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment 
      analyses. The protein-protein interaction network was constructed by STRING. 
      Overlapping targets were further analyzed using the online tool UALCAN to analyze 
      the correlation between gene expression and patient survival and prognosis. The 
      effect of ISO on OC cell proliferation, migration, and invasion was assessed in 
      vivo and in vitro, and the function of the estrogen receptor 1 (ESR1) in the 
      development of OC was examined by overexpressing and knocking down ESR1 
      expression. RESULTS: Through network pharmacology analysis, 25 target genes 
      related to ISO-OC were screened out. The overall survival rate of OC patients 
      only significantly correlated with high expression of ESR1 among 13 highly 
      expressed overlapping genes. ISO significantly inhibited the proliferation, 
      migration and invasion of OC cells in vitro and inhibited tumor growth in vivo. 
      Overexpression of ESR1 significantly promoted the proliferation, migration and 
      invasion of OC cells, whereas knockdown of ESR1 showed the opposite result. In 
      addition, overexpression of ESR1 significantly reversed the inhibitory effect of 
      ISO on the proliferation, migration and invasion of OC cells. CONCLUSIONS: We 
      confirmed that ISO inhibits OC cell proliferation, migration and invasion by 
      targeting ESR1 expression, which provides a theoretical basis for further 
      pharmacological research.
CI  - 2022 Annals of Translational Medicine. All rights reserved.
FAU - Wang, Manman
AU  - Wang M
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
FAU - Xu, Zhengtan
AU  - Xu Z
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
FAU - Cai, Qi
AU  - Cai Q
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
FAU - Deng, Yanmei
AU  - Deng Y
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
FAU - Shi, Weiqiao
AU  - Shi W
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
FAU - Zhou, Hongyu
AU  - Zhou H
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
FAU - Wang, Dajiang
AU  - Wang D
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
FAU - Li, Jian
AU  - Li J
AD  - Department of Pharmacy, West China Hospital of Sichuan University, Chengdu, 
      China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - Ann Transl Med
JT  - Annals of translational medicine
JID - 101617978
PMC - PMC9761148
OTO - NOTNLM
OT  - Estrogen receptor 1 (ESR1)
OT  - isorhamnetin (ISO)
OT  - network pharmacology
OT  - ovarian cancer (OC)
OT  - proliferation
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at 
      https://atm.amegroups.com/article/view/10.21037/atm-22-5064/coif). The authors 
      have no conflicts of interest to declare.
EDAT- 2022/12/23 06:00
MHDA- 2022/12/23 06:01
PMCR- 2022/11/01
CRDT- 2022/12/22 02:18
PHST- 2022/09/28 00:00 [received]
PHST- 2022/11/09 00:00 [accepted]
PHST- 2022/12/22 02:18 [entrez]
PHST- 2022/12/23 06:00 [pubmed]
PHST- 2022/12/23 06:01 [medline]
PHST- 2022/11/01 00:00 [pmc-release]
AID - atm-10-22-1216 [pii]
AID - 10.21037/atm-22-5064 [doi]
PST - ppublish
SO  - Ann Transl Med. 2022 Nov;10(22):1216. doi: 10.21037/atm-22-5064.