HMGA2-mediated tumorigenesis through angiogenesis in leiomyoma.


Journal

Fertility and sterility
ISSN: 1556-5653
Titre abrégé: Fertil Steril
Pays: United States
ID NLM: 0372772

Informations de publication

Date de publication:
11 2020
Historique:
received: 20 03 2020
revised: 25 05 2020
accepted: 28 05 2020
pubmed: 2 9 2020
medline: 19 5 2021
entrez: 2 9 2020
Statut: ppublish

Résumé

To study the role of HMGA2 in promoting angiogenesis in uterine leiomyoma (LM). This study involved evaluation of vessel density and angiogenic factors in leiomyomas with HMGA2 overexpression; examining angiogenic factor expression and AKT signaling in myometrial (MM) and leiomyoma cells by introducing HMGA2 overexpression in vitro; and exploring vessel formation induced by HMGA2 overexpression both in vitro and in vivo. University research laboratory. None. None. The main outcome measures include vessel density in leiomyomas with HMGA2 (HMGA2-LM) or MED12 (MED12-LM) alteration; angiogenic factor expression in primary leiomyoma and in vitro cell line model; and vessel formation in leiomyoma cells with HMGA2 overexpression in vitro and in vivo. Angiogenic factors and receptors were significantly upregulated at mRNA and protein levels in HMGA2-LM. Specifically, HMGA2-LM exhibited increased expression of VEGFA, EGF, bFGF, TGFα, VEGFR1, and VEGFR2 compared to MED12-LM and myometrium. Overexpression of HMGA2 in MM and LM cell lines resulted in increased secretion of angiogenesis-associated factors. Secreted factors promoted human umbilical vein endothelial cell (HUVEC) migration, tube formation, and wound healing. HMGA2 overexpression upregulated IGF2BP2 and pAKT, and silencing the IGF2BP2 gene reduced pAKT levels and reduced HUVEC migration. Myometrial cells with stable HMGA2 overexpression exhibited increased colony formation and cell growth in vitro and formed xenografts with increased blood vessels. HMGA2-LM have a high vasculature density, which likely contributes to tumor growth and disease burden of this leiomyoma subtype. HMGA2 plays an important role in angiogenesis and the involvement of IGF2BP2-mediated pAKT activity in angiogenesis, which provides a potential novel target for therapy for this subtype of LM.

Identifiants

pubmed: 32868105
pii: S0015-0282(20)30527-6
doi: 10.1016/j.fertnstert.2020.05.036
pmc: PMC7655683
mid: NIHMS1599719
pii:
doi:

Substances chimiques

HMGA2 Protein 0
HMGA2 protein, human 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1085-1096

Subventions

Organisme : NICHD NIH HHS
ID : P01 HD057877
Pays : United States
Organisme : NICHD NIH HHS
ID : P50 HD098580
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

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Auteurs

Yinuo Li (Y)

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Wenan Qiang (W)

Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Brannan Brooks Griffin (BB)

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Tingting Gao (T)

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Debabrata Chakravarti (D)

Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Serdar Bulun (S)

Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

J Julie Kim (JJ)

Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Jian-Jun Wei (JJ)

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. Electronic address: jianjun-wei@northwestern.edu.

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Classifications MeSH