PMID- 37859604
OWN - NLM
STAT- MEDLINE
DCOM- 20231113
LR  - 20231113
IS  - 1473-0766 (Electronic)
IS  - 0951-3590 (Linking)
VI  - 39
IP  - 1
DP  - 2023 Dec
TI  - Estrogen receptor-related receptor gamma uppresses hypoxia-induced angiogenesis by 
      regulating VEGFA in endometrial cancer.
PG  - 2264411
LID - 10.1080/09513590.2023.2264411 [doi]
AB  - OBJECTIVE: Estrogen receptor-related receptor gamma (ERRgamma), is implicated in cancer 
      cell proliferation and metastasis. The function of ERRgamma in tumor angiogenesis, 
      however, is to be revealed. This study was designed to elaborate the regulatory 
      effect of ERRgamma on angiogenesis in endometrial cancer (EC). METHODS: 
      Immunohistochemistry (IHC) was adopted to determine the protein expression of 
      ERRgamma, VEGFA, CD31 and hypoxia-inducible factor-1 (HIF-1) in tumor tissues. HEC-1A 
      cells stably expressing ERRgamma were established bytransfection, and then an 
      endothelial cell tube formation assay was performed. CCK-8 assay was employed for 
      cell viability, and wound healing assay for cell migration ability. Besides, 
      western blot, ELISA and qRT-PCR were used to examine the VEGFA expression. After 
      hypoxia treatment of ERRgamma overexpressing HEC-1A cells, the ERRgamma expression and 
      VEGFA expression were determined by western blot. Finally, EC xenografts in nude 
      mice were constructed by subcutaneous injection of ERRgamma stably expressing HEC-1A 
      cells and control HEC-1A cells. RESULTS: IHC results revealed a negative 
      correlation between the expression of ERRgamma and VEGFA in EC tissues. ERRgamma 
      overexpression significantly decreased the level of HIF-1 in tumor tissue of nude 
      mice. ERRgamma overexpression down-regulated inhibited angiogenesis capability and 
      inhibited the proliferation and migration of HEC-1A cells. Furthermore, ERRgamma 
      expression was suppressed under the condition of hypoxia while restoration of 
      ERRgamma partially inhibited hypoxia-induced VEGFA expression in HEC-1A cells. 
      CONCLUSIONS: ERRgamma is an angiogenesis suppressor and involved in hypoxia-induced 
      VEGFA expression in EC. Hence, ERRgamma might be a promising antiangiogenic target 
      for human EC.
FAU - Wang, Xiao-Xiao
AU  - Wang XX
AD  - Department of Gynecology, Women's Hospital, School of Medicine, Zhejiang 
      University, Hangzhou, China.
FAU - Hua, Teng
AU  - Hua T
AD  - Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan,China.
FAU - Wang, Hong-Bo
AU  - Wang HB
AD  - Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan,China.
LA  - eng
PT  - Journal Article
DEP - 20231020
PL  - England
TA  - Gynecol Endocrinol
JT  - Gynecological endocrinology : the official journal of the International Society 
      of Gynecological Endocrinology
JID - 8807913
RN  - 0 (ESRRG protein, human)
RN  - 0 (Receptors, Estrogen)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1)
SB  - IM
MH  - Animals
MH  - Female
MH  - Humans
MH  - Mice
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - *Endometrial Neoplasms/blood supply/genetics/metabolism/pathology
MH  - Hypoxia
MH  - Mice, Nude
MH  - *Neovascularization, Pathologic/genetics/metabolism
MH  - Receptors, Estrogen/metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
MH  - Hypoxia-Inducible Factor 1/metabolism
OTO - NOTNLM
OT  - Endometrial cancer (EC)
OT  - angiogenesis
OT  - estrogen receptor-related receptor gamma (ERRgamma)
OT  - hypoxia
OT  - vascular endothelial growth factor A (VEGFA)
EDAT- 2023/10/20 06:42
MHDA- 2023/10/23 01:18
CRDT- 2023/10/20 04:14
PHST- 2023/10/23 01:18 [medline]
PHST- 2023/10/20 06:42 [pubmed]
PHST- 2023/10/20 04:14 [entrez]
AID - 10.1080/09513590.2023.2264411 [doi]
PST - ppublish
SO  - Gynecol Endocrinol. 2023 Dec;39(1):2264411. doi: 10.1080/09513590.2023.2264411. 
      Epub 2023 Oct 20.