Nucleostemin promotes the proliferation of human glioma via Wnt/β-Catenin pathway
Corresponding Author
Zhen Bao
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Correspondence: Gang Cui, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China. Email: [email protected]Search for more papers by this authorYunfeng Wang
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorLixiang Yang
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorLin Wang
Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorLianxin Zhu
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorNa Ban
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorShaochen Fan
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorWenjuan Chen
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorJie Sun
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorChaoyan Shen
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorGang Cui
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorCorresponding Author
Zhen Bao
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Correspondence: Gang Cui, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China. Email: [email protected]Search for more papers by this authorYunfeng Wang
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorLixiang Yang
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorLin Wang
Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorLianxin Zhu
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorNa Ban
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorShaochen Fan
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorWenjuan Chen
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorJie Sun
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorChaoyan Shen
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, People's Republic of China
Search for more papers by this authorGang Cui
Departments of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China
Search for more papers by this authorAbstract
Nucleostemin, nucleolar guanosine triphosphate (GTP)-binding protein 3, is a member of the MMR1/HSR1 GTP-binding protein family. The important roles of nucleostemin in self-renewal, cell cycle regulation, apoptosis, and cell proliferation of various cancer types as been shown. Nevertheless, its expression and potential functions in human glioma is still unclear. In the present study, we demonstrated that up-regulation of nucleostemin was tightly related to poor 5-year-survival ratios. In serum-starved and re-feeding models of U251 and U373MG, we observed the rising expression of nucleostemin and p-β-Catenin (p-Tyr645) were accompanied with cell proliferation markers (cyclin D1 and proliferating cell nuclear antigen (PCNA)). Employing nucleostemin-depletion models, we found down-regulated nucleostemin and p-β-Catenin. The flow cytometry analysis proved the weakened cell proliferation. Moreover, we detected the translocation of β-Catenin into the nucleus was impaired, meaning the inhibition of the Wnt/β-Catenin pathway. Taken together, we identified a positive correlation between up-regulation of nucleostemin and human glioma cell proliferation and that knocking-down nucleostemin alleviated glioma proliferation by reducing β-Catenin transportation into the nucleus. All results suggested that nucleostemin might accelerate human glioma proliferation via the Wnt/β-Catenin pathway.
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