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479 results on '"Hu, Dan-Ning"'

4. Figures S1-S6 from SKP2 Activation by Thyroid Hormone Receptor β2 Bypasses Rb-Dependent Proliferation in Rb-Deficient Cells

Author

Xu, Xiaoliang L., primary, Li, Zhengke, primary, Liu, Aihong, primary, Fan, Xianqun, primary, Hu, Dan-ning, primary, Qi, Dong-Lai, primary, Chitty, David W., primary, Jia, Renbing, primary, Qui, Jianping, primary, Wang, Justin Q., primary, Sharaf, Jake, primary, Zou, Jun, primary, Weiss, Rebecca, primary, Huang, Hongyan, primary, Joseph, Walter J., primary, Ng, Lily, primary, Rosen, Richard, primary, Shen, Binghui, primary, Reid, Mark W., primary, Forrest, Douglas, primary, Abramson, David H., primary, Singer, Samuel, primary, Cobrinik, David, primary, and Jhanwar, Suresh C., primary

Published
2023
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5. Extended Methods, Reagents and Antibodies used, from SKP2 Activation by Thyroid Hormone Receptor β2 Bypasses Rb-Dependent Proliferation in Rb-Deficient Cells

Author

Xu, Xiaoliang L., primary, Li, Zhengke, primary, Liu, Aihong, primary, Fan, Xianqun, primary, Hu, Dan-ning, primary, Qi, Dong-Lai, primary, Chitty, David W., primary, Jia, Renbing, primary, Qui, Jianping, primary, Wang, Justin Q., primary, Sharaf, Jake, primary, Zou, Jun, primary, Weiss, Rebecca, primary, Huang, Hongyan, primary, Joseph, Walter J., primary, Ng, Lily, primary, Rosen, Richard, primary, Shen, Binghui, primary, Reid, Mark W., primary, Forrest, Douglas, primary, Abramson, David H., primary, Singer, Samuel, primary, Cobrinik, David, primary, and Jhanwar, Suresh C., primary

Published
2023
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18. miR-142-3p suppresses uveal melanoma by targeting CDC25C, TGFβR1, GNAQ, WASL, and RAC1

Author

Peng, Dewei, Dong, Jing, Zhao, Yunping, Peng, Xiaomei, Tang, Jingjing, Chen, Xiaoyan, Wang, Lihua, Hu, Dan-Ning, Reinach, Peter S, Qu, Jia, and Yan, Dongsheng

Subjects
tumor suppressor, miR-142-3p, molecular mechanisms, uveal melanoma, Original Research
Abstract

Purpose: Uveal melanoma (UM) is the most frequent metastatic ocular tumor in adults. Therapeutic intervention remains ineffective since none of the novel procedures used to treat this disease increased survival rates. To deal with this limitation, additional studies are required to clarify its pathogenesis. The current study focused on describing how epigenetic modulation by miR-142-3p affects changes in some cellular functions underlying UM pathogenesis. Methods and results: Microarray analysis identified 374 miRNAs which were differentially expressed between UM cells and uveal melanocytes. miR-142-3p was one of the 10 most downregulated miRNAs. Quantitative RT-PCR analysis confirmed that miR-142-3p expression levels were significantly decreased in both UM cell lines and clinical specimens. The results of the MTS, clone formation, scratch wound, transwell assays, and in vivo biofluorescence imaging showed that miR-142-3p overexpression significantly inhibited cell proliferation, migration, and invasiveness. Nevertheless, miR-142-3p did not affect cell apoptotic activity or sensitivity to doxorubicin. Cell cycle and EdU analysis showed that miR-142-3p overexpression induced G1/G2 cell cycle arrest and reduced DNA synthesis in UM cells. Microarray analysis showed that miR-142-3p mainly regulates the TGFβ signaling pathway, and those in which MAPK and PI3K-Akt are constituents. Functional interactions between miR-142-3p and CDC25C, TGFβR1, GNAQ, WASL, and RAC1 target genes were confirmed based on the results of the luciferase reporter assay and Western blot analysis. CDC25C or RAC1 downregulation is in agreement with cell cycle arrest and DNA synthesis disorder induction, while downregulation of TGFβR1, GNAQ, WASL, or RAC1 accounts for declines in cell migration. Conclusion: miR-143-3p is a potential therapeutic target to treat UM since overriding its declines in expression that occur in this disease reversed the pathogenesis of this disease. Such insight reveals novel biomarker for decreasing UM vitality and for improved tracking of tumor progression.

Published
2019

21. NSUN2-mediated RNA m5C modification modulates uveal melanoma cell proliferation and migration.

Author

Luo, Guangying, Xu, Weiwei, Chen, Xiaoyan, Wang, Siqi, Wang, Jiao, Dong, Feng, Hu, Dan-Ning, Reinach, Peter S., and Yan, Dongsheng

Subjects
RNA modification & restriction, CELL proliferation, RNA methylation, MELANOMA, CELL migration, METABOLIC regulation, RNA metabolism
Abstract

RNA 5-methylcytosine (m5C) is a widespread post-transcriptional modification involved in diverse biological processes through controlling RNA metabolism. However, its roles in uveal melanoma (UM) remain unknown. Here, we describe the biological roles and regulatory mechanisms of RNA m5C in UM. Initially, we identified significantly elevated global RNA m5C levels in both UM cells and tissue specimens using ELISA assay and dot blot analysis. Meanwhile, NOP2/Sun RNA methyltransferase family member 2 (NSUN2) was upregulated in both types of these samples, whereas NSUN2 knockdown significantly decreased RNA m5C level. Such declines inhibited UM cell migration and suppressed cell proliferation through cell cycle G1 arrest. Furthermore, bioinformatic analyses, m5C-RIP-qPCR, and luciferase assay identified β-Catenin (CTNNB1) as a direct target of NSUN2-mediated m5C modification in UM cells. Additionally, overexpression of miR-124a in UM cells diminished NSUN2 expression levels indicating that it is an upstream regulator of this response. Our study suggests that NSUN2-mediated RNA m5C methylation provides a potential novel target to improve the therapeutic management of UM pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2022
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33. Cover Image, Volume 235, Number 10, October 2020

Author

Luo, Guangying, primary, Xu, Weiwei, additional, Zhao, Yunping, additional, Jin, Shanshan, additional, Wang, Siqi, additional, Liu, Qi, additional, Chen, Xiaoyan, additional, Wang, Jiao, additional, Dong, Feng, additional, Hu, Dan‐Ning, additional, Reinach, Peter S., additional, and Yan, Dongsheng, additional

Published
2020
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