دورية أكاديمية
Downregulation of β-catenin blocks fibrosis via Wnt2 signaling in human keloid fibroblasts
العنوان: | Downregulation of β-catenin blocks fibrosis via Wnt2 signaling in human keloid fibroblasts |
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المؤلفون: | Yumei Cai, Shize Zhu, Weiqun Yang, Mingmeng Pan, Chaoyang Wang, Wenyi Wu |
المصدر: | Tumor Biology, Vol 39 (2017) |
بيانات النشر: | IOS Press, 2017. |
سنة النشر: | 2017 |
المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
مصطلحات موضوعية: | Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282 |
الوصف: | 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. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1423-0380 10104283 |
Relation: | https://doaj.org/toc/1423-0380 |
DOI: | 10.1177/1010428317707423 |
URL الوصول: | https://doaj.org/article/090299243058433a92ae4890c6e9363f |
رقم الأكسشن: | edsdoj.090299243058433a92ae4890c6e9363f |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 14230380 10104283 |
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DOI: | 10.1177/1010428317707423 |