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20 results on '"Miao, Yudi"'

2. MiR 26 targeting methyltetrahydrofolate reductase inhibits the proliferation of acute myeloid leukemia cells via JAK/STAT pathway

Author

Miao, Yudi, Zhao, Qiaojiajie, and Li, Chengliang

Subjects
miRNA, Leukemia, Proliferation, Apoptosis, Pharmaceutical Science, Pharmacology (medical)
Abstract

Purpose: To investigate the effect of microribonucleic acid (miR)-26 targeting methyltetrahydrofolate reductase (MTHFR) on cell proliferation, cycle, and apoptosis in acute myeloid leukemia (AML).Methods: The expressions of miR-26 in three types of human AML cell lines (HL-60, Kasumi-1, and KG-1a) and normal myeloid cell line (HS-5) were determined via quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR), while the effect of the over-expression of miR-26 on the proliferation, cell cycle and apoptosis of AML cells was evaluated using cell counting kit-8 (CCK-8) assay and flow cytometry. The potential target for miR-26 was predicted using public miRNA database TargetScan, and whether miR-26 binds to the predicted target was determined using a dual-luciferase reporter assay. Western blotting was performed to determine the effect of miR-26 on Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway-associated proteins.Results: Expression level of miR-26 was significantly lower in all AML cell lines than in HS-5 cells (p < 0.05). Overexpression of miR-26 inhibited the proliferation of KG-1a cells, reduced the percentage of cells in S phase, increased those in G0/G1 phase, and enhanced apoptosis of KG-1a cells (p < 0.05). After overexpression of miR-26, protein expression levels of phosphorylated (p)-JAK and p-STAT were down-regulated, while those of JAK and STAT did not change significantly.Conclusion: Expression of miR-26 is down-regulated in AML, while MiR-26 targeting of MTHFR induces apoptosis and cycle arrest of AML cells through the JAK/STAT pathway, thus inhibiting AML cell proliferation in vitro.

Published
2023

7. Clinical Efficacy Observation of Humanized BCMA-CAR-T in the Treatment of Relapsed/Refractory Multiple Myeloma Complicated with Extramedullary Lesions

Author

Wang, Yi, primary, Wang, Hui, additional, Niu, Ben, additional, Gao, Ying, additional, Zhang, Ding, additional, Miao, Yudi, additional, Zhou, Wei, additional, Hou, Limin, additional, Zhang, Hong, additional, Hu, Xingxing, additional, Wang, Fangyuan, additional, Li, Lan, additional, Ru, Xingli, additional, Zhang, Weihua, additional, Li, Xiang, additional, and Guan, Feng, additional

Published
2022
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20. Generation of dual-attribute iTNK cells from hPSCs for cancer immunotherapy

Author

Zhang, Yingfeng, He, Yuanyuan, Dai, Chenyi, Zhou, Zhengyang, Miao, Yudi, Zhao, Zixin, Lei, Qi, Li, Cheng, Wang, Chengyan, and Deng, Hongkui

Abstract

Dual-attribute immune cells possess advantageous features of cytotoxic T cells and natural killer (NK) cells and hold promise for advancing immunotherapy. Dual-attribute cell types such as invariant natural killer T cells, induced T-to-NK cells, and cytokine-induced killer cells have demonstrated efficacy and safety in preclinical and clinical studies. However, their limited availability hinders their widespread application. Human pluripotent stem cells (hPSCs) offer an ideal source. Here, we generate dual-attribute induced T-NK (iTNK) cells from hPSCs, expressing markers of both cytotoxic T and NK cells. Single-cell RNA and T cell receptor (TCR) sequencing analyses reveal that iTNK cells expressed signature genes associated with both NK and T cells and displayed a diverse TCR repertoire. iTNK cells release cytotoxic mediators, exert cytotoxicity against diverse tumor cell lines, and inhibit tumor growth in vivo. By harnessing adaptive and innate immune responses, hPSC-derived iTNK cells offer promising strategies for cancer immunotherapy.

Published
2024
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