The Natural Compound Neobractatin Induces Cell Cycle Arrest Through Multiple Signaling Pathways Including RNA Binding Protein CELF6

2018 ◽  
Author(s):  
Zhaoqing Zheng ◽  
Man Wu ◽  
Juan Zhang ◽  
Wenwei Fu ◽  
Naihan Xu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Signaling Pathways ◽  
Natural Compound ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Cycle Arrest ◽  
Multiple Signaling

scholarly journals The RNA-binding protein SART3 promotes miR-34a biogenesis and G1 cell cycle arrest in lung cancer cells

2019 ◽  
Vol 294 (46) ◽  
pp. 17188-17196 ◽  
Author(s):  
Emily J. Sherman ◽  
Dylan C. Mitchell ◽  
Amanda L. Garner
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Mirna Biogenesis ◽  
Regulatory Pathways ◽  
Cycle Arrest

MicroRNAs (miRNAs or miRs) are small, noncoding RNAs that are implicated in the regulation of most biological processes. Global miRNA biogenesis is altered in many cancers, and RNA-binding proteins play a role in miRNA biogenesis, presenting a promising avenue for targeting miRNA dysregulation in diseases. miR-34a exhibits tumor-suppressive activities by targeting cell cycle regulators CDK4/6 and anti-apoptotic factor BCL-2, among other regulatory pathways such as Wnt, TGF-β, and Notch signaling. Many cancers exhibit down-regulation or loss of miR-34a, and synthetic miR-34a supplementation has been shown to inhibit tumor growth in vivo. However, the post-transcriptional mechanisms that cause miR-34a loss in cancer are not entirely understood. Here, using a proteomics-mediated approach in non-small-cell lung cancer (NSCLC) cells, we identified squamous cell carcinoma antigen recognized by T-cells 3 (SART3) as a putative pre-miR-34a–binding protein. SART3 is a spliceosome recycling factor and nuclear RNA-binding protein with no previously reported role in miRNA regulation. We found that SART3 binds pre-miR-34a with higher specificity than pre-let-7d (used as a negative control) and elucidated a new functional role for SART3 in NSCLC cells. SART3 overexpression increased miR-34a levels, down-regulated the miR-34a target genes CDK4/6, and caused a cell cycle arrest in the G1 phase. In vitro binding experiments revealed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Our results provide evidence for a significant role of SART3 in miR-34a biogenesis and cell cycle progression in NSCLC cells.

scholarly journals MCG10, a Novel p53 Target Gene That Encodes a KH Domain RNA-Binding Protein, Is Capable of Inducing Apoptosis and Cell Cycle Arrest in G2-M

2000 ◽  
Vol 20 (15) ◽  
pp. 5602-5618 ◽  
Author(s):  
Jianhui Zhu ◽  
Xinbin Chen
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Target Gene ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Wild Type ◽  
Cycle Arrest ◽  
Kh Domain ◽  
P53 Target Gene

ABSTRACT p53, a tumor suppressor, inhibits cell proliferation by inducing cellular genes involved in the regulation of the cell cycle.MCG10, a novel cellular p53 target gene, was identified in a cDNA subtraction assay with mRNA isolated from a p53-producing cell line. MCG10 can be induced by wild-type but not mutant p53 and by DNA damage via two potential p53-responsive elements in the promoter of the MCG10 gene. The MCG10 gene contains 10 exons and is located at chromosome 3p21, a region highly susceptible to aberrant chromosomal rearrangements and deletions in human neoplasia. The MCG10 gene locus encodes at least two alternatively spliced transcripts, MCG10 and MCG10as. The MCG10 and MCG10as proteins contain two domains homologous to the heterogeneous nuclear ribonucleoprotein K homology (KH) domain. By generating cell lines that inducibly express either wild-type or mutated forms of MCG10 and MCG10as, we found that MCG10 and MCG10as can suppress cell proliferation by inducing apoptosis and cell cycle arrest in G2-M. In addition, we found that MCG10 and MCG10as, through their KH domains, can bind poly(C) and that their RNA-binding activity is necessary for inducing apoptosis and cell cycle arrest. Furthermore, we found that the level of the poly(C) binding MCG10 protein is increased in cells treated with the DNA-damaging agent camptothecin in a p53-dependent manner. These results suggest that the MCG10 RNA-binding protein is a potential mediator of p53 tumor suppression.

Signaling pathways involved in cell cycle arrest during the DNA breaks

DNA Repair ◽  
2021 ◽  
Vol 98 ◽  
pp. 103047
Author(s):  
Fatemeh Sadoughi ◽  
Jamal Hallajzadeh ◽  
Zatollah Asemi ◽  
Mohammad Ali Mansournia ◽  
Forough Alemi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Signaling Pathways ◽  
Dna Breaks ◽  
Cycle Arrest

scholarly journals The Natural Compound Neobractatin Induces Cell Cycle Arrest by Regulating E2F1 and Gadd45α

2019 ◽  
Vol 9 ◽  
Author(s):  
Zhaoqing Zheng ◽  
Man Wu ◽  
Juan Zhang ◽  
Wenwei Fu ◽  
Naihan Xu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Natural Compound ◽  
Cycle Arrest

scholarly journals Glioblastoma Multiforme Stem Cell Cycle Arrest by Alkylaminophenol through the Modulation of EGFR and CSC Signaling Pathways

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 681 ◽  
Author(s):  
Phuong Doan ◽  
Aliyu Musa ◽  
Akshaya Murugesan ◽  
Vili Sipilä ◽  
Nuno R. Candeias ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cell ◽  
Glioblastoma Multiforme ◽  
Cell Cycle Arrest ◽  
Signaling Pathways ◽  
Cell Lines ◽  
Cell Population ◽  
Significant Role ◽  
Dependent Manner ◽  
Cycle Arrest

Cancer stem cells (CSCs), a small subpopulation of cells existing in the tumor microenvironment promoting cell proliferation and growth. Targeting the stemness of the CSC population would offer a vital therapeutic opportunity. 3,4-Dihydroquinolin-1(2H)-yl)(p-tolyl)methyl)phenol (THTMP), a small synthetic phenol compound, is proposed to play a significant role in controlling the CSC proliferation and survival. We assessed the potential therapeutic effects of THTMP on glioblastoma multiforme (GBM) and its underlying mechanism in various signaling pathways. To fully comprehend the effect of THTMP on the CSCs, CD133+ GBM stem cell (GSC) and CD133- GBM Non-stem cancer cells (NSCC) population from LN229 and SNB19 cell lines was used. Cell cycle arrest, apoptosis assay and transcriptome analysis were performed for individual cell population. THTMP strongly inhibited NSCC and in a subtle way for GSC in a time-dependent manner and inhibit the resistance variants better than that of temozolomide (TMZ). THTMP arrest the CSC cell population at both G1/S and G2/M phase and induce ROS-mediated apoptosis. Gene expression profiling characterize THTMP as an inhibitor of the p53 signaling pathway causing DNA damage and cell cycle arrest in CSC population. We show that the THTMP majorly affects the EGFR and CSC signaling pathways. Specifically, modulation of key genes involved in Wnt, Notch and Hedgehog, revealed the significant role of THTMP in disrupting the CSCs’ stemness and functions. Moreover, THTMP inhibited cell growth, proliferation and metastasis of multiple mesenchymal patient-tissue derived GBM-cell lines. THTMP arrests GBM stem cell cycle through the modulation of EGFR and CSC signaling pathways.

scholarly journals The TIA1 RNA-Binding Protein Family Regulates EIF2AK2-Mediated Stress Response and Cell Cycle Progression

2018 ◽  
Vol 69 (4) ◽  
pp. 622-635.e6 ◽  
Author(s):  
Cindy Meyer ◽  
Aitor Garzia ◽  
Michael Mazzola ◽  
Stefanie Gerstberger ◽  
Henrik Molina ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stress Response ◽  
Cell Cycle Progression ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Protein Family ◽  
Cycle Progression

scholarly journals A Novel Role for the RNA–Binding Protein FXR1P in Myoblasts Cell-Cycle Progression by Modulating p21/Cdkn1a/Cip1/Waf1 mRNA Stability

PLoS Genetics ◽  
2013 ◽  
Vol 9 (3) ◽  
pp. e1003367 ◽  
Author(s):  
Laetitia Davidovic ◽  
Nelly Durand ◽  
Olfa Khalfallah ◽  
Ricardo Tabet ◽  
Pascal Barbry ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mrna Stability ◽  
Cell Cycle Progression ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Cycle Progression

Phosphorylation of RNA-binding protein controls cell cycle switch from mitotic to meiotic in fission yeast

Nature ◽  
1997 ◽  
Vol 386 (6621) ◽  
pp. 187-190 ◽  
Author(s):  
Yoshinori Watanabe ◽  
Satoko Shinozaki-Yabana ◽  
Yuji Chikashige ◽  
Yasushi Hiraoka ◽  
Masayuki Yamamoto
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein
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