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Two serine residues of non-metastasis protein 23-H1 are critical in inhibiting signal transducer and activator of transcription 3 activity in human lung cancer cells.

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机构: [1]Department of Medical Biology, Wannan Medical College, Wuhu, Anhui 241002 [2]Tianjin Key Laboratoryof Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Center and Institute,Tianjin Medical University General Hospital, Tianjin 300052 [3]Laboratory of Cancer Cell Biology,Tianjin Medical University Cancer Institute and Hospital, Hexi, Tianjin 300060 [4]Department of Central Laboratory,Wannan Medical College, Wuhu, Anhui 241002 [5]Sichuan Lung Cancer Institute, Sichuan Lung Cancer Center,West China Hospital, Sichuan University, Chengdu, Sichuan 610000, P.R. China
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关键词: non‑metastasis protein 23‑H1 metastasis signal transducer and activator of transcription 3 protein inhibitor of activated signal transducer and activator of transcription 3 non‑small‑cell lung cancer

摘要:
Constitutive activation of signal transducer and activator of transcription 3 (STAT3) in numerous cancers, including lung cancer, is one of the major mechanisms of tumor progression and metastasis. The authors previously reported that the metastasis suppressor non-metastasis protein 23-H1 (Nm23-H1) negatively regulates STAT3 activity by inhibiting its phosphorylation on Tyr705. Nm23-H1 is a multifunction protein that has three different kinase activities. By transfecting the five mutants that inactivated three different kinase activities respectively into Nm23-H1 deficient lung cancer cell lines, it was identified that Nm23-H1S44A (Ser44 to Ala) and Nm23-H1S120G (Ser120 to Gly) mutant forms were unable to suppress STAT3 phosphorylation on Tyr705, resulting in increased expression of fibronectin and matrix metalloproteinase-9. Notably, protein inhibitor of activated STAT3 was also involved in Nm23-H1S44A- and Nm23-H1S120G-mediated suppression of STAT3 phosphorylation. The present results indicated that Ser44 and Ser120 sites of Nm23-H1 may be responsible for its biological suppressive effects of STAT3 and tumor metastasis, which may contribute to illuminate the metastasis suppression function of Nm23-H1 in lung cancer.

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出版当年[2017]版:
大类 | 4 区 医学
小类 | 4 区 肿瘤学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 肿瘤学
第一作者:
第一作者机构: [1]Department of Medical Biology, Wannan Medical College, Wuhu, Anhui 241002 [*1]Department of Medical Biology, Wannan Medical College, 22 Wenchang West Road, Wuhu, Anhui 241002, P.R. China
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通讯机构: [1]Department of Medical Biology, Wannan Medical College, Wuhu, Anhui 241002 [2]Tianjin Key Laboratoryof Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Center and Institute,Tianjin Medical University General Hospital, Tianjin 300052 [5]Sichuan Lung Cancer Institute, Sichuan Lung Cancer Center,West China Hospital, Sichuan University, Chengdu, Sichuan 610000, P.R. China [*1]Department of Medical Biology, Wannan Medical College, 22 Wenchang West Road, Wuhu, Anhui 241002, P.R. China [*2]Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Center and Institute, Tianjin Medical University General Hospital, 154 Anshan Road, Heping, Tianjin 300052, P.R. China
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