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Downregulation of β-catenin blocks fibrosis via Wnt2 signaling in human keloid fibroblasts.

Abstract Keloid is a disorder of fibroproliferative diseases that occurs in wounds, characterized by an exaggerated response to injury. The key factor responsible for the disease process has not been identified. This study sought to elucidate the role of β-catenin in the regulation of keloid phenotypes and signaling. Expression of β-catenin in keloid and normal non-keloid samples was measured by real-time polymerase chain reaction. Knockdown of β-catenin was achieved by delivering small interfering RNA to target β-catenin. Cell proliferation, cell cycle progression, and apoptosis of keloid cells were measured by functional assays in vitro. The proteins related to keloid fibrosis were measured by Western blotting. β-catenin expression was significantly upregulated in keloid tissue samples compared with the normal non-keloid age-adjusted skin sample counterparts. Functionally, targeting β-catenin with lipofection-delivered small interfering RNA oligonucleotide inhibited the proliferation and cell cycle arrest in G0/G1 phase and increased apoptosis of fibroblast cells, accompanied by downregulation of Wnt2 and cyclin D1 as well as the phosphorylation level of glycogen synthase kinase 3 beta in the keloid fibrosis. Our study supports a crucial role of β-catenin in the regulation of fibroproliferation and extracellular matrix deposition. Targeting β-catenin using small interfering RNA oligonucleotide may be a promising approach for preventing excessive fibroproliferative development after wound healing and may lead to the development of novel strategies for restoring keloid diseases.
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Authors

Mayor MeshTerms
Keywords

Keloid

Wnt2 pathway

cell proliferation

fibroblast

β-catenin

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




PMID- 28656880
OWN - NLM
STAT- In-Process
DA  - 20170628
LR  - 20170628
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Downregulation of beta-catenin blocks fibrosis via Wnt2 signaling in human keloid
      fibroblasts.
PG  - 1010428317707423
LID - 10.1177/1010428317707423 [doi]
AB  - Keloid is a disorder of fibroproliferative diseases that occurs in wounds,
      characterized by an exaggerated response to injury. The key factor responsible
      for the disease process has not been identified. This study sought to elucidate
      the role of beta-catenin in the regulation of keloid phenotypes and signaling.
      Expression of beta-catenin in keloid and normal non-keloid samples was measured
      by real-time polymerase chain reaction. Knockdown of beta-catenin was achieved by
      delivering small interfering RNA to target beta-catenin. Cell proliferation, cell
      cycle progression, and apoptosis of keloid cells were measured by functional
      assays in vitro. The proteins related to keloid fibrosis were measured by Western
      blotting. beta-catenin expression was significantly upregulated in keloid tissue 
      samples compared with the normal non-keloid age-adjusted skin sample
      counterparts. Functionally, targeting beta-catenin with lipofection-delivered
      small interfering RNA oligonucleotide inhibited the proliferation and cell cycle 
      arrest in G0/G1 phase and increased apoptosis of fibroblast cells, accompanied by
      downregulation of Wnt2 and cyclin D1 as well as the phosphorylation level of
      glycogen synthase kinase 3 beta in the keloid fibrosis. Our study supports a
      crucial role of beta-catenin in the regulation of fibroproliferation and
      extracellular matrix deposition. Targeting beta-catenin using small interfering
      RNA oligonucleotide may be a promising approach for preventing excessive
      fibroproliferative development after wound healing and may lead to the
      development of novel strategies for restoring keloid diseases.
FAU - Cai, Yumei
AU  - Cai Y
AD  - 1 Department of Pathology, Quanzhou Medical College, Quanzhou, China.
FAU - Zhu, Shize
AU  - Zhu S
AD  - 2 Department of Plastic Surgery, The Second Affiliated Hospital of Fujian Medical
      University, Quanzhou, China.
FAU - Yang, Weiqun
AU  - Yang W
AD  - 1 Department of Pathology, Quanzhou Medical College, Quanzhou, China.
FAU - Pan, Mingmeng
AU  - Pan M
AD  - 2 Department of Plastic Surgery, The Second Affiliated Hospital of Fujian Medical
      University, Quanzhou, China.
FAU - Wang, Chaoyang
AU  - Wang C
AD  - 2 Department of Plastic Surgery, The Second Affiliated Hospital of Fujian Medical
      University, Quanzhou, China.
FAU - Wu, Wenyi
AU  - Wu W
AD  - 2 Department of Plastic Surgery, The Second Affiliated Hospital of Fujian Medical
      University, Quanzhou, 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
OTO - NOTNLM
OT  - Keloid
OT  - Wnt2 pathway
OT  - cell proliferation
OT  - fibroblast
OT  - beta-catenin
EDAT- 2017/06/29 06:00
MHDA- 2017/06/29 06:00
CRDT- 2017/06/29 06:00
AID - 10.1177/1010428317707423 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317707423. doi: 10.1177/1010428317707423.