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紫杉醇通过介导PI3K/AKT/mTOR信号通路来减少FLT3-ITD急性髓系白血病细胞的增殖并促进其凋亡。

Paclitaxel mediates the PI3K/AKT/mTOR pathway to reduce proliferation of FLT3‑ITD AML cells and promote apoptosis.

作者信息

Su Yanyun, Wu Meiqing, Zhou Baowen, Bai Ziwen, Pang Ruli, Liu Zhenfang, Zhao Weihua

机构信息

Department of Hematology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.

出版信息

Exp Ther Med. 2024 Feb 23;27(4):161. doi: 10.3892/etm.2024.12449. eCollection 2024 Apr.

DOI:10.3892/etm.2024.12449
PMID:38476887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10928971/
Abstract

Acute myeloid leukemia (AML) with internal tandem duplication (ITD) mutations in the FLT3 tyrosine kinase tend to have a poor prognosis. FLT3-ITD can promote the progress of AML by activating the PI3K/AKT/mTOR pathway. Paclitaxel (PTX) is a natural anticancer drug that has been widely used in chemotherapy for multiple malignancies. The present study used the CCK-8 assay, flow cytometry, PCR and western blotting to explore the anti-leukemia effect and possible mechanisms of PTX on MV4-11 cells with the FLT3-ITD mutation and the underlying mechanism. As a result, it was found that PTX could inhibit proliferation of MV4-11 cells and promoted apoptosis by inhibiting the PI3K/AKT/mTOR pathway.

摘要

伴有FLT3酪氨酸激酶内部串联重复（ITD）突变的急性髓系白血病（AML）往往预后较差。FLT3-ITD可通过激活PI3K/AKT/mTOR通路促进AML进展。紫杉醇（PTX）是一种天然抗癌药物，已广泛用于多种恶性肿瘤的化疗。本研究采用CCK-8法、流式细胞术、PCR和蛋白质印迹法，探讨PTX对具有FLT3-ITD突变的MV4-11细胞的抗白血病作用、可能机制及潜在机制。结果发现，PTX可抑制MV4-11细胞增殖，并通过抑制PI3K/AKT/mTOR通路促进细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/7acdecb84874/etm-27-04-12449-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/4d22c196fabd/etm-27-04-12449-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/addc4e2b67b4/etm-27-04-12449-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/0c72c154a885/etm-27-04-12449-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/254736f16345/etm-27-04-12449-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/0a5da133cbad/etm-27-04-12449-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/54f345b1e124/etm-27-04-12449-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/d6bbf186d770/etm-27-04-12449-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/7acdecb84874/etm-27-04-12449-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/4d22c196fabd/etm-27-04-12449-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/addc4e2b67b4/etm-27-04-12449-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/0c72c154a885/etm-27-04-12449-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/254736f16345/etm-27-04-12449-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/0a5da133cbad/etm-27-04-12449-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/54f345b1e124/etm-27-04-12449-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/d6bbf186d770/etm-27-04-12449-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e05/10928971/7acdecb84874/etm-27-04-12449-g07.jpg

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