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TRIM22 knockdown suppresses chronic myeloid leukemia via inhibiting PI3K/Akt/mTOR signaling pathway

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机构: [1]Department of Hematology, Yunnan Research Center of Hematology, the First Affiliated Hospital of Kunming Medical University, Kunming, P. R.China [2]Department of Laboratory Medicine, Yuhuangding Hospital of Qingdao University, Yantai, P. R. China [3]Department of Clinical Laboratory, Yunnan Institute of Experimental Diagnosis, the First Affiliated Hospital of Kunming Medical University, YunnanKey Laboratory of Laboratory Medicine, No. 295, Xichang Road, Kunming City, Yunnan Province, P. R. China [4]Department of Thoracic Surgery, the First Affiliated Hospital of Kunming Medical University, Kunming, P. R. China [5]Department of Urinary Surgery, the First People’s Hospital of Kunming City, Kunming, P. R. China
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关键词: cancer chronic myeloid leukemia PI3K Akt mTOR pathway RNA interference (RNAi) TRIM22 tumor suppressor

摘要:
Tripartite motif-containing 22 (TRIM22) is reported to participate in numerous cellular activities. Recent studies confirm that TRIM22 is a target gene for P53, and inhibits clonogenic growth of leukemic U-937 cells. The current study aims to discover the effect of TRIM22 in progression of human chronic myeloid leukemia (CML) and explore the related mechanism. TRIM22 was knocked down by siRNA transfection in CML cell K562. We observed that TRIM22 knockdown decreased proliferation and invasion in K562 cells. TRIM22 knockdown significantly induced cell cycle arrest by regulating the level of CDK4, Cyclin D1, P70S6K, and P53 in K562 cell. Moreover, loss of TRIM22 also promoted apoptosis through modulation of Bcl-2, Bax and active Caspase 3 in K562 cell. Furthermore, we demonstrated that TRIM22 knockdown inhibited the activation of PI3K/Akt/mTOR pathway by decreasing the level of the phosphorylated form p-Akt and p-mTOR in K562 cell. In conclusion, loss of TRIM22 suppresses the progression and invasion of CML through regulation of PI3K/Akt/mTOR pathway, suggesting that TRIM22 might be as a potential target for the treatment strategy of CML.

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出版当年[2019]版:
大类 | 4 区 生物
小类 | 4 区 细胞生物学
最新[2023]版:
大类 | 3 区 生物学
小类 | 4 区 细胞生物学
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出版当年[2018]版:
Q4 CELL BIOLOGY
最新[2023]版:
Q3 CELL BIOLOGY

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第一作者机构: [1]Department of Hematology, Yunnan Research Center of Hematology, the First Affiliated Hospital of Kunming Medical University, Kunming, P. R.China
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