Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

2011 ◽  
Vol 294 (8) ◽  
pp. 1337-1343 ◽  
Author(s):  
Li Zhao ◽  
Zhi-Hua Wen ◽  
Chun-Hong Jia ◽  
Ming Li ◽  
Shen-Qiu Luo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

scholarly journals TRAF2 Knockdown in Nasopharyngeal Carcinoma Induced Cell Cycle Arrest and Enhanced the Sensitivity to Radiotherapy

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Hongyuan Zhu ◽  
Weijun Ding ◽  
Jiaojiao Wu ◽  
Rongyou Ma ◽  
Zhaohu Pan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Cell Cycle Arrest ◽  
Transcriptional Activity ◽  
Adaptor Protein ◽  
Biological Functions ◽  
Xenograft Tumor ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

TRAF2 is a crucial adaptor protein involved in various signaling pathways. However, its biological functions in nasopharyngeal carcinoma (NPC) remain largely unknown. In the present study, we found that TRAF2 was overexpressed in nasopharyngeal carcinoma (NPC) cells. Knockdown of TRAF2 with shRNA significantly suppressed NPC cell proliferation and colony formation. The growth of xenograft tumor significantly reduced after TRAF2 was silenced. Conversely, the ectopic overexpression of TRAF2 significantly promoted cell proliferation and anchorage-independent growth. In TRAF2 knockdown cells, EGF-induced activation of transcriptional factors, including MSK1, CREB, and ATF2, markedly decreased. Accordingly, the transcriptional activity of AP-1 was substantially decreased in TRAF2-deficient cells. With the suppression of gene transcription, the expression of cyclin D1 was significantly impaired, which gave rise to the G0/G1 cell cycle arrest. Moreover, the overexpression of TRAF2 in NPC cells was associated with resistance to irradiation, and the potency of irradiation was substantially enhanced after TRAF2 was knocked down. Briefly, our studies demonstrated that TRAF2 had a crucial role in NPC development, and it might be of great potential to targeting TRAF2 for NPC prevention and treatment.

scholarly journals Induction of p53-Independent Apoptosis and G1 Cell Cycle Arrest by Fucoidan in HCT116 Human Colorectal Carcinoma Cells

Marine Drugs ◽  
2017 ◽  
Vol 15 (6) ◽  
pp. 154 ◽  
Author(s):  
Hye Park ◽  
Shin-Hyung Park ◽  
Jin-Woo Jeong ◽  
Dahye Yoon ◽  
Min Han ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Human Colorectal Carcinoma

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

Antimalarial agent artesunate induces G0/G1 cell cycle arrest and apoptosis via increasing intracellular ROS levels in normal liver cells

2020 ◽  
Vol 39 (12) ◽  
pp. 1681-1689
Author(s):  
S Yin ◽  
H Yang ◽  
X Zhao ◽  
S Wei ◽  
Y Tao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Normal Liver ◽  
Liver Cells ◽  
Phase Cell ◽  
Normal Cells ◽  
Cycle Arrest ◽  
Intracellular Ros ◽  
G1 Cell Cycle Arrest

Artesunate (ARS) has been shown to be highly effective against chloroquine-resistant malaria. In vitro studies reported that ARS has anticancer effects; however, its detrimental action on cancer cells may also play a role in its toxicity toward normal cells and its potential toxicity has not been sufficiently researched. In this study, we investigated the possible cytotoxic effects using normal BRL-3A and AML12 liver cells. The results showed that ARS dose-dependently inhibited cell proliferation and arrested the G0/G1 phase cell cycle in both BRL-3A and AML12 liver cells. Western blotting demonstrated that ARS induced a significant downregulation of cyclin-dependent kinase-2 (CDK2), CDK4, cyclin D1, and cyclin E1 in various levels and then caused apoptosis when the Bcl-2/Bax ratio decreased. Conversely, the levels of intracellular reactive oxygen species (ROS) were increased. The ROS scavenger N-acetylcysteine can significantly inhibit cell cycle arrest and apoptosis induced by ARS. Thus, the data confirmed that ARS exposure impairs normal liver cell proliferation by inducing G0/G1 cell cycle arrest and apoptosis, and this detrimental action may be associated with intracellular ROS accumulation. Collectively, the possible side effects of ARS on healthy normal cells cannot be neglected when developing therapies.

scholarly journals Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells

2013 ◽  
Vol 29 (6) ◽  
pp. 2101-2108 ◽  
Author(s):  
KEFENG WU ◽  
YI LIU ◽  
YINGNIAN LV ◽  
LIAO CUI ◽  
WENDE LI ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nasopharyngeal Carcinoma ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Cycle Arrest

Antifibrotic Agent Pirfenidone Suppresses Proliferation of Human Pancreatic Cancer Cells by Inducing G0/G1 Cell Cycle Arrest

Pharmacology ◽  
2019 ◽  
Vol 103 (5-6) ◽  
pp. 250-256 ◽  
Author(s):  
Eri Usugi ◽  
Kenichiro Ishii ◽  
Yoshifumi Hirokawa ◽  
Kazuki Kanayama ◽  
Chise Matsuda ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Experimental Conditions ◽  
Cycle Arrest ◽  
Pancreatic Cancer Cells ◽  
G1 Cell Cycle Arrest

Background: Pirfenidone (PFD), which is an antifibrotic agent used for treatment of idiopathic pulmonary fibrosis, induces G0/G1 cell cycle arrest in fibroblasts. We hypothesized that PFD-induced G0/G1 cell cycle arrest might be achieved in other types of cells, including cancer cells. Here we investigated the effects of PFD on the proliferation of pancreatic cancer cells (PCCs) in vitro. Method: Human skin fibroblasts ASF-4-1 cells and human prostate stromal cells (PrSC) were used as fibroblasts. PANC-1, MIA PaCa-2, and BxPC-3 cells were used as human PCCs. Cell cycle and apoptosis were analyzed using flow cytometer. Results: First, we confirmed that PFD suppressed cell proliferation of ASF-4-1 cells and PrSC and induced G0/G1 cell cycle arrest. Under these experimental conditions, PFD also suppressed cell proliferation and induced G0/G1 cell cycle arrest in all PCCs. In PFD-treated PCCs, expression of p21 was increased but that of CDK2 was not clearly decreased. Of note, PFD did not induce significant apoptosis among PCCs. Conclusions: These results demonstrated that the antifibrotic agent PFD might have antiproliferative effects on PCCs by inducing G0/G1 cell cycle arrest. This suggests that PFD may target not only fibroblasts but also PCCs in the tumor microenvironment of pancreatic cancer.

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