Nucleostemin promotes the proliferation of human glioma via Wnt/β‐Catenin pathway

Bao, Zhen; Wang, Yunfeng; Yang, Lixiang; Wang, Lin; Zhu, Lianxin; Ban, Na; Fan, Shaochen; Chen, Wenjuan; Sun, Jie; Shen, Chaoyan; Cui, Gang

doi:10.1111/neup.12265

Cited by 14 publications

(13 citation statements)

References 38 publications

(73 reference statements)

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“…These results also indicated that inhibition of ribosome biogenesis might disrupt oncology pathways thus inhibit cell proliferation and promote apoptosis of PTC. This proposition is consistent with the report that neucleolar protein Nucleostemin promoted cell proliferation of human glioma via Wnt/β-Catenin pathway [ 25 ], suggesting abnormal expression of nucleolar protein could active oncology pathway.…”

Section: Discussionsupporting

confidence: 93%

RRS1 gene expression involved in the progression of papillary thyroid carcinoma

Chen

Jin

et al. 2018

Cancer Cell Int

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BackgroundPapillary thyroid carcinoma (PTC) is one of the most frequent malignancies of the endocrine system, whose mechanisms of pathogenesis, progression and prognosis are still far from being clearly elucidated. Despite an increasing body of evidences highlights ribosome biogenesis regulator homolog (RRS1) as a ribosome biogenesis protein in yeast and plants, little is known about human RRS1 function.MethodsProliferation, cell cycle and apoptosis of PTC cells were assessed following the knockdown of RRS1 expression though MTT, colony formation assay, and flow cytometry. Then, transcriptome profiling was conducted to explore pathway changes after RRS1 silencing in PTC cells. Receiver operating characteristic curve and Youden’s index were performed in twenty-four thyroid carcinoma samples to assess their potential clinical diagnostic value.ResultsFirstly, we found that silencing RRS1 significantly reduced cell proliferation, inhibited cell cycle, and promoted apoptosis in PTC cell line. The result also showed that knock-down of RRS1 could up-regulate genes involving apoptosis and metabolism, while, down-regulate genes relative to cell proliferation and blood vessel development. Notably, the present study confirmed the diagnostic value of RRS1 for thyroid carcinoma in both children and adults.ConclusionsIn conclusion, these data afford a comprehensive view of a novel function of human RRS1 by promoting cell proliferation and could be a potential indicator for papillary thyroid carcinoma.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0519-x) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 93%

RRS1 gene expression involved in the progression of papillary thyroid carcinoma

Chen

Jin

et al. 2018

Cancer Cell Int

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“…These data were also confirmed in Wnt10B knockdown cells, demonstrating that reduced Wnt10B expression also downregulated expression of Oct4 and Nanog in gastric cancer cells in vitro . Further studies may confirm whether Wnt10B knockdown inhibits β-catenin translocation into cell nuclei, as shown by previous studies in other cancers (35–38). …”

Section: Discussionsupporting

confidence: 78%

Wnt10B is critical for the progression of gastric cancer

Bie

Zhang

et al. 2017

Oncology Letters

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The family of Wnt proteins have been implicated in embryogenesis by regulation of cell fate and pattern formation, and also in human carcinogenesis. Wnt10B was previously shown to be involved in breast cancer development. The present study assessed the association of Wnt10B expression in human gastric cancer tissue specimens with clinicopathological data from these patients. Wnt10B expression in the regulation of gastric cancer cell proliferation and migration capacity in vitro was then investigated. The data revealed that Wnt10B mRNA and protein were upregulated in gastric cancer tissue samples and the upregulated Wnt10B mRNA was associated with gastric cancer metastasizing to lymph nodes. Knockdown of Wnt10B expression reduced gastric cancer cell proliferation and migration, as well as expression of a cell proliferation marker Ki67. Knockdown of Wnt10B expression inhibited tumor cell epithelial-mesenchymal transition by upregulation of E-cadherin and downregulation of N-cadherin. In addition, Wnt10B knockdown also suppressed tumor cell stemness by downregulation of octamer-binding transcription factor 4 and Nanog expression. The present data indicated that Wnt10B expression performs an important role in gastric cancer progression in vitro. Therefore, targeting of Wnt10B expression or activity may be investigated as a possible strategy for the control of gastric cancer.

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“…However, it is noteworthy that there are inconsistent reports regarding the cell cycle arrest caused by GNL3 dysregulation in different tumor cells. It is demonstrated that GNL3 knockdown triggers cell cycle arrest at the G1 phase in hepatocellular carcinoma HepG2 and Hep3B cells,12 ovarian cancer SKOV-3 cells,13 and glioma U251 and U373MG cells 19. Conversely, Meng et al20 claim that GNL3 knockdown triggers G2-M arrest in U2OS cells, while overexpression of GNL3 is revealed to induce G1 arrest through inhibiting MDM2 in U2OS cells 21.…”

Section: Discussionmentioning

confidence: 99%

<p>The oncogenic role of GNL3 in the progression and metastasis of osteosarcoma</p>

Li¹,

Long²,

Wu³

et al. 2019

CMAR

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BackgroundGNL3 has been reported to be up-regulated in cancers and function in tumor progression, whereas the role of GNL3 in the progression of osteosarcoma remains unclear.Materials and methodsIn this study, we blocked the expression of GNL3 by siRNA interference in osteosarcoma cell lines MG63 and U20S. CCK8, colony formation, wound-healing, Transwell, flow cytometry, and Hoechst/PI staining assays were used to examine the effects of GNL3 knockdown on cell proliferation, migration, invasion and apoptosis in MG63 and U20S cells. The relative activity of MMP9 was detected using Gelatin zymography assay. Western blot was performed to detect the expression of related proteins.ResultsWe found that silencing of GNL3 reduced the growth, migration, and invasion abilities of MG63 and U20S cells. Moreover, silencing GNL3 triggered cell cycle arrest in MG63 and U20S cells, as well as promoted cell apoptosis. In addition, depletion of GNL3 was observed to reduce the activity of MMP9 and suppress the process of epithelial–mesenchymal transition (EMT) through up-regulation of E-cadherin and down-regulation of N-cadherin. Furthermore, we found that X-box-binding protein 1 (XBP1) could bind to GNL3 using dual-luciferase reporter assay, and XBP1 overexpression could restore the inhibitory effects on proliferation, invasion, and EMT in MG63 and U20S cells caused by GNL3 knockdown.ConclusionThese data suggest that GNL3 functions as an oncogene in the progression of osteosarcoma by regulation of EMT, and XBP1 is also involved in its mechanism.

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Nucleostemin promotes the proliferation of human glioma via Wnt/β‐Catenin pathway

Cited by 14 publications

References 38 publications

RRS1 gene expression involved in the progression of papillary thyroid carcinoma

RRS1 gene expression involved in the progression of papillary thyroid carcinoma

Wnt10B is critical for the progression of gastric cancer

<p>The oncogenic role of GNL3 in the progression and metastasis of osteosarcoma</p>

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