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175 results on '"Li, Meng-qi"'

12. Concomitant Gallstone Disease was not Associated with Long‐term Outcomes in Ursodeoxycholic Acid‐treated Patients with Primary Biliary Cholangitis

Author

Chen, Sha, primary, Li, Meng Qi, additional, Li, Bu Er, additional, Lv, Ting Ting, additional, Li, Shu Xiang, additional, Shan, Shan, additional, Li, Min, additional, Kong, Yuan Yuan, additional, Zhang, Dong, additional, Ma, Hong, additional, Ou, Xiao Juan, additional, You, Hong, additional, Duan, Wei Jia, additional, and Jia, Ji Dong, additional

Published
2023
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17. β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases

Author

Gao, Ping-ping, Li, Ling, Chen, Ting-ting, Li, Nan, Li, Meng-qi, Zhang, Hui-juan, Chen, Ya-ning, Zhang, Shi-hao, Wei, Wei, and Sun, Wu-yi

Abstract

β-arrestin2, a pivotal protein within the arrestin family, is localized in the cytoplasm, plasma membrane and nucleus, and regulates G protein-coupled receptors (GPCRs) signaling. Recent evidence shows that β-arrestin2 plays a dual role in regulating GPCRs by mediating desensitization and internalization, and by acting as a scaffold for the internalization, kinase activation, and the modulation of various signaling pathways, including NF-κB, MAPK, and TGF-β pathways of non-GPCRs. Earlier studies have identified that β-arrestin2 is essential in regulating immune cell infiltration, inflammatory factor release, and inflammatory cell proliferation. Evidently, β-arrestin2 is integral to the pathological mechanisms of inflammatory immune diseases, such as inflammatory bowel disease, sepsis, asthma, rheumatoid arthritis, organ fibrosis, and tumors. Research on the modulation of β-arrestin2 offers a promising strategy for the development of pharmaceuticals targeting inflammatory immune diseases. This review meticulously describes the roles of β-arrestin2 in cells associated with inflammatory immune responses and explores its pathological relevance in various inflammatory immune diseases.

Published
2024
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22. In Situ Methylammonium Chloride-Assisted Perovskite Crystallization Strategy for High-Performance Solar Cells

Author

Zuo, Wei-Wei, primary, Yang, Ying-Guo, additional, Fu, Wei-Fei, additional, Li, Meng, additional, Malekshahi Byranvand, Mahdi, additional, Di Girolamo, Diego, additional, Pascual, Jorge, additional, Li, Meng-Qi, additional, Li, Li−Na, additional, Abate, Antonio, additional, Saliba, Michael, additional, and Wang, Zhao-Kui, additional

Published
2022
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37. MiR-214 inhibits cell migration, invasion and promotes the drug sensitivity in human cervical cancer by targeting FOXM1

Author

Wang, Jian-Mei, Ju, Bao-Hui, Pan, Cai-Jun, Gu, Yan, Li, Meng-Qi, Sun, Li, Xu, Yan-Ying, and Yin, Li-Rong

Subjects
Original Article
Abstract

Object: MicroRNAs (miRNAs) play key roles in progression of cervical cancer. In the present study, we investigated the role of miR-214 in the process of migration, invasion and drug sensitivity to cisplatin in cervical cancer. Methods: We detected the differential expression of miR-214 in 19 cases cervical cancer tissues and normal tissues as well as 4 cervical cancer cells and one normal cervical cells by Real-time PCR. Then, wound healing assay, transwell invasion assay and MTT were used to detect the effects of migration, invasion and sensitivity to cisplatin of cervical cancer when miR-214 was overexpressed. Western blot, immunofluorescence and Flow Cytometry were used to detect the mechanism of migration, invasion and sensitivity to cisplatin. Next, bioinformatics analysis was used to find the target of miR-214. Through the luciferase reporter assay, Real-time PCR and western blot, we confirmed the binding relationship of miR-214 and FOXM1. In cervical cancer tissues, the expression of FOXM1 was detected by western blot and Immunohistochemistry. We also knocked down FOXM1 in cervical cancer cells, wound healing assay, transwell invasion assay and MTT were performed to detect the migration, invasion and sensitivity to cisplatin abilities of FOXM1. Western blot and Flow Cytometry were used to detect the mechanism of migration, invasion and sensitivity to cisplatin by FOXM1. Finally, we performed rescue expriments to confirm the function relationship between miR-214 and FOXM1. Results: 1. Our results showed that miR-214 was frequently downregulated in tumor tissues and cancer cells especially in CIN III and cervical cancer stages. 2. Overexpression of miR-214 significantly inhibited migration and invasion of cervical cancer cells and prompted the sensitivity to cisplatin. 3. FOXM1 was identified as a target of miR-214 and down-regulated by miR-214. 4. Knocking down FOXM1 could inhibited migration and invasion of cervical cancer cells and prompted the sensitivity to cisplatin. 5. FOXM1 was upregulated in tumor tissues. 6. The mechanism of migration, invasion and sensitivity to cisplatin were the resluts of changes of EMT and apoptosis. 7. The restoration of FOXM1 expression can counteract the effect of miR-214 on cell migration, invasion and sensitivity to cisplatin of cervical cancer cells. Conclusions: These findings indicate that miR-214 acts as a tumor suppressor during the process of migration, invasion and drug sensitivity through targeting FOXM1, suggesting miR-214 as a potential new diagnostic and therapeutic target for the treatment of cervical cancer.

Published
2017

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