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Angiotensin II type 2 receptor-interacting protein 3a inhibits ovarian carcinoma metastasis via the extracellular HMGA2-mediated ERK/EMT pathway.

Abstract Local migration and long-distance metastasis is the main reason for higher mortality of ovarian cancer. Microtubule-associated tumor suppressor 1/angiotensin II type 2 receptor-interacting protein is associated with tumor initiation and progression and exerts anti-tumor effects. High mobility group AT-hook 2 is overexpressed in majority of metastatic carcinomas, which contributes to carcinomas metastasis through Snail-induced epithelial-to-mesenchymal transition signal pathway. The purpose of this study was to investigate the signal pathway of microtubule-associated tumor suppressor 1/angiotensin II type 2 receptor-interacting protein-mediated anti-tumor effects. Our data observed that ovarian carcinoma cells exhibited lower expression of angiotensin II type 2 receptor-interacting protein 3a and higher expression of high mobility group AT-hook 2 compared to normal ovarian cells. Restoration of angiotensin II type 2 receptor-interacting protein 3a expression in ovarian carcinoma cells inhibited high mobility group AT-hook 2 expression and exhibited anti-proliferative effects. In addition, angiotensin II type 2 receptor-interacting protein 3a treatment suppressed the phosphorylation of epithelial-to-mesenchymal transition and extracellular signal-regulated kinase in ovarian carcinoma cells. We also observed that angiotensin II type 2 receptor-interacting protein 3a restoration downregulated expression of Snail, E-Cadherin, N-Cadherin, and Vimentin in ovarian carcinoma cells, whereas angiotensin II type 2 receptor-interacting protein 3a knockdown enhanced the phosphorylation of extracellular signal-regulated kinase and epithelial-to-mesenchymal transition. In vivo assay indicated that angiotensin II type 2 receptor-interacting protein 3a inhibited ovarian tumor growth and elevated survival of tumor-bearing immunodeficient mice. Tumor histological analysis indicated that Snail, E-Cadherin, N-Cadherin, and Vimentin expression levels were downregulated via decreasing high mobility group AT-hook 2 expression. Furthermore, upregulation of angiotensin II type 2 receptor-interacting protein 3a impaired the phenotype of extracellular signal-regulated kinase and epithelial-to-mesenchymal transition in ovarian carcinoma cells and tumor tissues. Taken together, angiotensin II type 2 receptor-interacting protein 3a presents potential in suppressing the proliferation and aggressiveness of ovarian carcinoma cells through the high mobility group AT-hook 2-mediated extracellular signal-regulated kinase/epithelial-to-mesenchymal transition signal pathway.
PMID
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Authors

Mayor MeshTerms
Keywords

Ovarian carcinoma

angiotensin II type 2 receptor–interacting protein 3a

extracellular signal–regulated kinase/epithelial-to-mesenchymal transition

high mobility group AT-hook 2

metastasis

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28651497
OWN - NLM
STAT- MEDLINE
DA  - 20170627
DCOM- 20170710
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Angiotensin II type 2 receptor-interacting protein 3a inhibits ovarian carcinoma 
      metastasis via the extracellular HMGA2-mediated ERK/EMT pathway.
PG  - 1010428317713389
LID - 10.1177/1010428317713389 [doi]
AB  - Local migration and long-distance metastasis is the main reason for higher
      mortality of ovarian cancer. Microtubule-associated tumor suppressor
      1/angiotensin II type 2 receptor-interacting protein is associated with tumor
      initiation and progression and exerts anti-tumor effects. High mobility group
      AT-hook 2 is overexpressed in majority of metastatic carcinomas, which
      contributes to carcinomas metastasis through Snail-induced
      epithelial-to-mesenchymal transition signal pathway. The purpose of this study
      was to investigate the signal pathway of microtubule-associated tumor suppressor 
      1/angiotensin II type 2 receptor-interacting protein-mediated anti-tumor effects.
      Our data observed that ovarian carcinoma cells exhibited lower expression of
      angiotensin II type 2 receptor-interacting protein 3a and higher expression of
      high mobility group AT-hook 2 compared to normal ovarian cells. Restoration of
      angiotensin II type 2 receptor-interacting protein 3a expression in ovarian
      carcinoma cells inhibited high mobility group AT-hook 2 expression and exhibited 
      anti-proliferative effects. In addition, angiotensin II type 2
      receptor-interacting protein 3a treatment suppressed the phosphorylation of
      epithelial-to-mesenchymal transition and extracellular signal-regulated kinase in
      ovarian carcinoma cells. We also observed that angiotensin II type 2
      receptor-interacting protein 3a restoration downregulated expression of Snail,
      E-Cadherin, N-Cadherin, and Vimentin in ovarian carcinoma cells, whereas
      angiotensin II type 2 receptor-interacting protein 3a knockdown enhanced the
      phosphorylation of extracellular signal-regulated kinase and
      epithelial-to-mesenchymal transition. In vivo assay indicated that angiotensin II
      type 2 receptor-interacting protein 3a inhibited ovarian tumor growth and
      elevated survival of tumor-bearing immunodeficient mice. Tumor histological
      analysis indicated that Snail, E-Cadherin, N-Cadherin, and Vimentin expression
      levels were downregulated via decreasing high mobility group AT-hook 2
      expression. Furthermore, upregulation of angiotensin II type 2
      receptor-interacting protein 3a impaired the phenotype of extracellular
      signal-regulated kinase and epithelial-to-mesenchymal transition in ovarian
      carcinoma cells and tumor tissues. Taken together, angiotensin II type 2
      receptor-interacting protein 3a presents potential in suppressing the
      proliferation and aggressiveness of ovarian carcinoma cells through the high
      mobility group AT-hook 2-mediated extracellular signal-regulated
      kinase/epithelial-to-mesenchymal transition signal pathway.
FAU - Ping, Huang
AU  - Ping H
AD  - Department of Gynaecology, Cangzhou Central Hospital, Cangzhou, China.
FAU - Guo, Liang
AU  - Guo L
AD  - Department of Gynaecology, Cangzhou Central Hospital, Cangzhou, China.
FAU - Xi, Jie
AU  - Xi J
AD  - Department of Gynaecology, Cangzhou Central Hospital, Cangzhou, China.
FAU - Wang, Donghui
AU  - Wang D
AD  - Department of Gynaecology, Cangzhou Central Hospital, Cangzhou, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (HMGA2 Protein)
RN  - 0 (MTUS1 protein, human)
RN  - 0 (Tumor Suppressor Proteins)
SB  - IM
MH  - Animals
MH  - Carcinoma/*genetics/pathology
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Epithelial-Mesenchymal Transition/genetics
MH  - Female
MH  - HMGA2 Protein/*genetics
MH  - Humans
MH  - MAP Kinase Signaling System/genetics
MH  - Mice
MH  - Neoplasm Invasiveness/genetics/pathology
MH  - Neoplasm Metastasis
MH  - Ovarian Neoplasms/*genetics/pathology
MH  - Signal Transduction/genetics
MH  - Tumor Suppressor Proteins/*genetics
MH  - Xenograft Model Antitumor Assays
OTO - NOTNLM
OT  - Ovarian carcinoma
OT  - angiotensin II type 2 receptor-interacting protein 3a
OT  - extracellular signal-regulated kinase/epithelial-to-mesenchymal transition
OT  - high mobility group AT-hook 2
OT  - metastasis
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317713389 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317713389. doi: 10.1177/1010428317713389.