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miRNA-mediated TUSC3 deficiency enhances UPR and ERAD to promote metastatic potential of NSCLC.

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机构： [1]Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA. [2]Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. [3]Department of Biology, Stanford University, Stanford, CA 94305, USA. [4]Institute for Cellular and Molecular Biology, Center for Systems and Synthetic Biology, The University of Texas at Austin, Austin, TX 78712, USA. [5]Department of Pathology, Stanford University, Stanford, CA 94305, USA. [6]Department of Biosciences, Mokpo National University, Muan 58554, South Korea. [7]Departments of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. [8]Department of Animal Science, College of Agriculture and Life Sciences, Chonnam National University, Gwangju 61186, Korea. [9]Gwangju Center, Korea Basic Science Institute, Gwangju 61186, Korea. [10]Department of Life System, Sookmyung Woman’s University, Seoul 140-742, Republic of Korea. [11]Department of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, 610041 Chengdu, China. [12]Transcriptional Networks in Lung Cancer Group, Cancer Research United Kingdom Manchester Institute, University of Manchester, Manchester M20 4BX, United Kingdom. [13]Department of Cancer Biology and Genetics, The Ohio State University, Columbus, OH 43210, USA. [14]School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035 Zhejiang, China. [15]Department of Neurosurgery UAB Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA. [16]Departments of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA. [17]Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Medical Oncology, The Ohio State University, Columbus, OH 43210, USA.

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Non-small cell lung carcinoma (NSCLC) is leading cause of cancer-related deaths in the world. The Tumor Suppressor Candidate 3 (TUSC3) at chromosome 8p22 known to be frequently deleted in cancer is often found to be deleted in advanced stage of solid tumors. However, the role of TUSC3 still remains controversial in lung cancer and context-dependent in several cancers. Here we propose that miR-224/-520c-dependent TUSC3 deficiency enhances the metastatic potential of NSCLC through the alteration of three unfolded protein response pathways and HRD1-dependent ERAD. ATF6α-dependent UPR is enhanced whereas the affinity of HRD1 to its substrates, PERK, IRE1α and p53 is weakened. Consequently, the alteration of UPRs and the suppressed p53-NM23H1/2 pathway by TUSC3 deficiency is ultimately responsible for enhancing metastatic potential of lung cancer. These findings provide mechanistic insight of unrecognized roles of TUSC3 in cancer progression and the oncogenic role of HRD1-dependent ERAD in cancer metastasis.

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出版当年[2018]版：

大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

最新[2023]版：

大类 | 1 区

综合性期刊

小类 | 1 区综合性期刊

第一作者：

第一作者机构： [1]Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA. [2]Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.

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通讯作者：

通讯机构： [1]Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA. [13]Department of Cancer Biology and Genetics, The Ohio State University, Columbus, OH 43210, USA. [14]School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035 Zhejiang, China.

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