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Liquiritigenin exerts the anti-cancer role in oral cancer via inducing autophagy-related apoptosis through PI3K/AKT/mTOR pathway inhibition in vitro and in vivo.
Ji, Yingchen; Hu, Weiwei; Jin, Yan; Yu, Huiming; Fang, Jin.
Afiliação
  • Ji Y; Department of Stomatology, Jiangsu Provincial Hospital of Traditional Chinese Medicine, Jiangsu, 210029, China.
  • Hu W; Department of Stomatology, Huai'an Second People's Hospital and Affiliated Huai'an Hospital of Xuzhou Medical University, Jiangsu, China.
  • Jin Y; Department of Medical Oncology, Affiliated Huai'an No.1 People's Hospital, Nanjing Medical University, Jiangsu, China.
  • Yu H; Department of Stomatology, Jiangsu Provincial Hospital of Traditional Chinese Medicine, Jiangsu, 210029, China.
  • Fang J; Department of Stomatology, Affiliated Huai'an No.1 People's Hospital, Nanjing Medical University, Jiangsu, China.
Bioengineered ; 12(1): 6070-6082, 2021 12.
Article em En | MEDLINE | ID: mdl-34488535
Operative treatment on oral cancer greatly damages the chewing and language function of the patient, we aim to find better solution with fewer side effects. The anti-tumor effects of Liquiritigenin (LQ) have been explored in kinds of cancers, but not in oral cancer. In this study, our purpose is to reveal the effects of LQ on oral cancer and the associated mechanism.Cell proliferation was examined through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and 5-Ethynyl-2'- deoxyuridine (EDU) staining. Cell apoptosis in cells and tissues were assessed by flow cytometry and terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. Expressions of AKT and light chain 3 (LC3) were detected through Immunofluorescence. In addition, xenograft model was established by injecting the CAL-27 cells (2 × 106) subcutaneously into the right flanks of mice. Expression of Ki67 and Beclin1 in tissues was valued by Immunohistochemistry (IHC).We found that cell viability of CAL-27 and SCC-9 was effectively inhibited by LQ. Besides, obvious cell apoptosis and cell autophagy were induced by LQ. In addition, PI3K/AKT/mTOR pathway was sharply inactivated by LQ in oral cancer cells. Corresponding in vivo experiments demonstrated that tumor growth was largely restricted, cell apoptosis was augmented and autophagy was enhanced by LQ. What is more, phosphorylation of AKT in tumor tissues could also be inhibited by LQ. LQ inhibited the progression of oral cancer through inducing autophagy-associated apoptosis via PI3K/AKT/mTOR pathway inhibition, revealing a new possible scheme for the treatment of oral cancer.
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Texto completo: 1 Base de dados: MEDLINE Medicinas Tradicionais: Medicinas_tradicionales_de_asia / Medicina_china Assunto principal: Autofagia / Neoplasias Bucais / Transdução de Sinais / Flavanonas / Antineoplásicos Idioma: En Revista: Bioengineered Ano de publicação: 2021 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Base de dados: MEDLINE Medicinas Tradicionais: Medicinas_tradicionales_de_asia / Medicina_china Assunto principal: Autofagia / Neoplasias Bucais / Transdução de Sinais / Flavanonas / Antineoplásicos Idioma: En Revista: Bioengineered Ano de publicação: 2021 Tipo de documento: Article País de afiliação: China