scholarly journals The Role of Bystander Effect in Ultraviolet A Induced Photoaging

2021 ◽  
Author(s):  
Surajit Hansda ◽  
Gargi Ghosh ◽  
Rita Ghosh
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Bystander Effect ◽  
Marker Genes ◽  
Uva Irradiation ◽  
Cycle Arrest ◽  
Normal Expression ◽  
Cox 2 ◽  
Bystander Cells ◽  
First Time

Abstract Background: Exposure to sunlight, mainly UVA, leads to typical changes in the features of the skin known as photoaging. UVA irradiation induces the expression of proteases that are responsible for the degradation of the extracellular matrix proteins to results in photoaging; it also downregulates the expression of proteins that are needed for the skin structure. Since, it is known that cells in the neighborhood of irradiated cells, but not directly exposed to it, often manifest responses like their irradiated counterparts, it is important to evaluate if these bystander cells too, can contribute to photoaging. Methods and Results: UVA induced cell cycle arrest have been associated with photoaging, from flow cytometry analysis we found that there was an induction of cell cycle arrest at the G1/S phase in the UVA-bystander cells. The expression of some key photoaging marker genes likes, matrix metalloproteinases (MMP-1, MMP-3, MMP-9), cyclooxygenase-2 (COX-2), collagen1 and elastin were assessed from qRT-PCR. Upregulation of MMP-1 and COX-2, downregulation of collagen1 and elastin, along with suppression below normal expression for MMP-3 and MMP-9 was observed in the UVA-bystander A375 cells. Conclusion: Our findings for the first time suggest the contribution of UVA-bystander cells to the process of photoaging.

scholarly journals Induction of G0/G1 cell cycle arrest in ovarian carcinoma cells by the anti-inflammatory drug NS-398, but not by COX-2-specific RNA interference

Oncogene ◽  
2003 ◽  
Vol 22 (54) ◽  
pp. 8653-8661 ◽  
Author(s):  
Carsten Denkert ◽  
Antje Fürstenberg ◽  
Peter Ted Daniel ◽  
Ines Koch ◽  
Martin Köbel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rna Interference ◽  
Ovarian Carcinoma ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Inflammatory Drug ◽  
Cycle Arrest ◽  
Ovarian Carcinoma Cells ◽  
G1 Cell Cycle Arrest ◽  
Cox 2

ASIC1A INHIBITOR MAMBALGIN-2 SUPPRESSES GROWTH OF LEUKEMIA CELLS BY CELL CYCLE ARREST

2020 ◽  
pp. 234-235
Author(s):  
V. Vasileva ◽  
A. Sudarikova ◽  
M. Kirpichnikov ◽  
E. Lyukmanova
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Leukemia Cells ◽  
Cycle Arrest ◽  
Gated Channel ◽  
First Time

For the first time the inhibitor of proton-gated channel ASIC1a was proposed as prototype of new anti-leukemic compound

COX‐2 independent induction of cell cycle arrest and apoptosis in colon cancer cells by the selective COX‐2 inhibitor celecoxib

2001 ◽  
Vol 15 (14) ◽  
pp. 1-22 ◽  
Author(s):  
Sabine Grösch ◽  
Irmgard Tegeder ◽  
Ellen Niederberger ◽  
Lutz Bräutigam ◽  
Gerd Geisslinger
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Cycle Arrest ◽  
Cox 2

scholarly journals Sinomenine, a COX-2 inhibitor, induces cell cycle arrest and inhibits growth of human colon carcinoma cells in vitro and in vivo

2015 ◽  
Vol 11 (1) ◽  
pp. 411-418 ◽  
Author(s):  
HAIBO YANG ◽  
PEIHAO YIN ◽  
ZHAN SHI ◽  
YANCHUN MA ◽  
CHENGGEN ZHAO ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Colon Carcinoma Cells ◽  
Cycle Arrest ◽  
Human Colon Carcinoma ◽  
Cox 2

scholarly journals Cidan inhibits liver cancer cell growth by reducing COX-2 and VEGF expression and cell cycle arrest

2015 ◽  
Vol 9 (5) ◽  
pp. 1709-1718 ◽  
Author(s):  
NAN LI ◽  
DONGHAI ZHENG ◽  
JIE XUE ◽  
WEIXING GUO ◽  
JIE SHI ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Liver Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Liver Cancer Cell ◽  
Vegf Expression ◽  
Cancer Cell Growth ◽  
Cycle Arrest ◽  
Cox 2

Celastrol inhibits the proliferation and induces apoptosis of colorectal cancer cells via downregulating NF-κB/COX-2 signaling pathways

2021 ◽  
Vol 21 ◽  
Author(s):  
Hua Zhang ◽  
Xiaojin Zhao ◽  
Fajun Shang ◽  
Huan Sun ◽  
Xu Zheng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Cycle Arrest ◽  
The World ◽  
Cox 2

Background: Colorectal cancer (CRC) is the third-ranked malignant tumor in the world that contributes to the death of a major population of the world. Celastrol, a bioactive natural product isolated from the medicinal plant Tripterygium wilfordii Hook F, has been proved to be an effective anti-tumor inhibitor for multiple tumors. Objective: To reveal the therapeutic effect and underlying mechanisms of celastrol on CRC cells. Methods: CCK-8 and clonogenic assay were used to analyze the cell proliferation in CRC cells. Flow cytometry analysis was conducted to assess the cell cycle and cell apoptosis. Wound-healing and cell invasion assay were used to evaluate the migrating and invasion capability of CRC cells. The potential antitumor mechanism of celastrol was investigated by qPCR, western blot, and confocal immunofluorescence analyses. Results: Celastrol effectively inhibited CRC cell proliferation by activating caspase-dependent cell apoptosis and facilitating G1 cell cycle arrest in a dose-dependent manner, as well as cell migration and invasion by downregulating the MMP2 and MMP9. Mechanistic protein expression revealed that celastrol suppressed the expression of COX-2 by inhibiting the phosphorylation of NF-κB p65 and subsequently leading to cytoplasmic retention of p65 protein, thereby inhibiting its nuclear translocation and transcription activities. Conclusion: These findings indicate that celastrol is an effective inhibitor for CRC, regulating the NF-κB/COX-2 pathway, leading to the inhibition of cell proliferation characterized by cell cycle arrest and caspase-dependent apoptosis, providing a potential alternative therapeutic agent for CRC patients.

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