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ARD1 contributes to IKK beta-mediated breast cancer tumorigenesis

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机构: [1]Department of Oncology, Guizhou Provincial People’s Hospital, 550002Guizhou, China [2]Department of Chemotherapy, Sichuan Cancer Hospital &Institute, Sichuan Cancer Center, School of Medicine, University of ElectronicScience and Technology of China, 610041 Chengdu, China [3]People’s Hospitalof Danzhai County, 557500 Guizhou, China [4]State Key Laboratory ofBiotherapy and Cancer Center, West China Hospital, Sichuan University andCollaborative Innovation Center for Biotherapy, 610041 Chengdu, China
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The expression of I.B kinase beta (IKK beta) promotes the growth of breast cancer cells. Meanwhile, IKK beta mediates the phosphorylation and subsequent degradation of arrest-defective protein 1 (ARD1). However, the relationship between IKK beta and ARD1 in the occurrence of breast cancer has not been reported. In this study, we found that IKK beta not only acts directly on mammalian target of rapamycin (mTOR) activity but also indirectly acts on mTOR activity through posttranscriptional modification of ARD1, thereby effectively promoting the growth of breast cancer cells. ARD1 prevents mTOR activity and breast cancer cell growth by stabilizing tuberous sclerosis complex 2 (TSC2) to induce autophagy. Moreover, acetylation of heat shock protein 70 (Hsp70) also contributes to ARD1-mediated autophagy. Therefore, upstream IKK beta can further promote the occurrence of breast cancer by mediating the function of ARD1.

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出版当年[2018]版:
大类 | 2 区 生物
小类 | 2 区 细胞生物学
最新[2023]版:
大类 | 1 区 生物学
小类 | 2 区 细胞生物学
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出版当年[2018]版:
Q1 CELL BIOLOGY
最新[2023]版:
Q1 CELL BIOLOGY

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第一作者机构: [1]Department of Oncology, Guizhou Provincial People’s Hospital, 550002Guizhou, China
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