scholarly journals Anticancer potential of nitric oxide (NO) in neuroblastoma treatment

RSC Advances ◽  
2021 ◽  
Vol 11 (16) ◽  
pp. 9112-9120
Author(s):  
Jenna L. Gordon ◽  
Kristin J. Hinsen ◽  
Melissa M. Reynolds ◽  
Tyler A. Smith ◽  
Haley O. Tucker ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Cycle ◽  
Cell Division ◽  
Cell Viability ◽  
Cell Cycle Arrest ◽  
Neuroblastoma Cells ◽  
Cycle Arrest

S-Nitrosoglutathione (GSNO) reduces cell viability, inhibits cell division, and induces cell cycle arrest and apoptosis in neuroblastoma cells.

(3,3’-Methylene)bis-2-hydroxy-1,4-naphthoquinones induce cytotoxicity against DU145 and PC3 cancer cells by inhibiting cell viability and promoting cell cycle arrest

2021 ◽  
Author(s):  
Paula Priscilla de Freitas ◽  
Ruan Carlos Busquet Ribeiro ◽  
Isabella dos Santos Guimarães ◽  
Caroline S. Moreira ◽  
David R. Rocha ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Viability ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cycle Arrest

Activation of the BRCA1/Chk1/p53/p21Cip1/Waf1 pathway by nitric oxide and cell cycle arrest in human neuroblastoma NB69 cells

Nitric Oxide ◽  
2012 ◽  
Vol 26 (3) ◽  
pp. 182-191 ◽  
Author(s):  
Marlies Van de Wouwer ◽  
Célia Couzinié ◽  
Miguel Serrano-Palero ◽  
Óscar González-Fernández ◽  
Clara Galmés-Varela ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Human Neuroblastoma ◽  
Cycle Arrest

scholarly journals The Role of Nitric Oxide in Cancer: Master Regulator or NOt?

2020 ◽  
Vol 21 (24) ◽  
pp. 9393
Author(s):  
Faizan H. Khan ◽  
Eoin Dervan ◽  
Dibyangana D. Bhattacharyya ◽  
Jake D. McAuliffe ◽  
Katrina M. Miranda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Cell Cycle Progression ◽  
Epithelial To Mesenchymal Transition ◽  
Tumour Microenvironment ◽  
Master Regulator ◽  
Mesenchymal Transition ◽  
Cycle Arrest

Nitric oxide (NO) is a key player in both the development and suppression of tumourigenesis depending on the source and concentration of NO. In this review, we discuss the mechanisms by which NO induces DNA damage, influences the DNA damage repair response, and subsequently modulates cell cycle arrest. In some circumstances, NO induces cell cycle arrest and apoptosis protecting against tumourigenesis. NO in other scenarios can cause a delay in cell cycle progression, allowing for aberrant DNA repair that promotes the accumulation of mutations and tumour heterogeneity. Within the tumour microenvironment, low to moderate levels of NO derived from tumour and endothelial cells can activate angiogenesis and epithelial-to-mesenchymal transition, promoting an aggressive phenotype. In contrast, high levels of NO derived from inducible nitric oxide synthase (iNOS) expressing M1 and Th1 polarised macrophages and lymphocytes may exert an anti-tumour effect protecting against cancer. It is important to note that the existing evidence on immunomodulation is mainly based on murine iNOS studies which produce higher fluxes of NO than human iNOS. Finally, we discuss different strategies to target NO related pathways therapeutically. Collectively, we present a picture of NO as a master regulator of cancer development and progression.

Cell-cycle arrest in TrkA-expressing NIH3T3 cells involves nitric oxide synthase

2001 ◽  
Vol 81 (1) ◽  
pp. 193-204 ◽  
Author(s):  
Dylan A. Bulseco ◽  
Wojciech Poluha ◽  
Christopher M. Schonhoff ◽  
Marie-Claire Daou ◽  
Peter J. Condon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Cycle ◽  
Nitric Oxide Synthase ◽  
Cell Cycle Arrest ◽  
Nih3t3 Cells ◽  
Cycle Arrest ◽  
Oxide Synthase

MicroRNA-1225-5p acts as a tumor-suppressor in laryngeal cancer via targeting CDC14B

2019 ◽  
Vol 400 (2) ◽  
pp. 237-246 ◽  
Author(s):  
Peng Sun ◽  
Dan Zhang ◽  
Haiping Huang ◽  
Yafeng Yu ◽  
Zhendong Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Division ◽  
Cell Cycle Arrest ◽  
Molecular Mechanisms ◽  
Normal Tissues ◽  
Cycle Arrest ◽  
Enhanced Expression ◽  
Insight Into

Abstract This study aimed to investigate the role of miRNA-1225-5p (miR-1225) in laryngeal carcinoma (LC). We found that the expression of miR-1225 was suppressed in human LC samples, while CDC14B (cell division cycle 14B) expression was reinforced in comparison with surrounding normal tissues. We also demonstrated that enhanced expression of miR-1225 impaired the proliferation and survival of LC cells, and resulted in G1/S cell cycle arrest. In contrast, reduced expression of miR-1225 promoted cell survival. Moreover, miR-1225 resulted in G1/S cell cycle arrest and enhanced cell death. Further, miR-1225 targets CDC14B 3′-UTR and recovery of CDC14B expression counteracted the suppressive influence of miR-1225 on LC cells. Thus, these findings offer insight into the biological and molecular mechanisms behind the development of LC.

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