scholarly journals Omeprazole Inhibits Cell Proliferation and Induces G0/G1 Cell Cycle Arrest through Up-regulating miR-203a-3p Expression in Barrett’s Esophagus Cells

2018 ◽  
Vol 8 ◽  
Author(s):  
Yichao Hou ◽  
Qiang Hu ◽  
Jiao Huang ◽  
Hua Xiong
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

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.

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.

A phenylacetate derivative, SCK6, inhibits cell proliferation via G1 cell cycle arrest and apoptosis

2003 ◽  
Vol 467 (1-3) ◽  
pp. 31-39 ◽  
Author(s):  
Hsu-Chin Chan ◽  
Sheng-Chu Kuo ◽  
Li-Jiau Huang ◽  
Chung-Hsien Liu ◽  
Shih-Lan Hsu
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
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 N-Octanoyl dopamine transiently inhibits T cell proliferation via G1 cell-cycle arrest and inhibition of redox-dependent transcription factors

2014 ◽  
Vol 96 (3) ◽  
pp. 453-462 ◽  
Author(s):  
Johannes Wedel ◽  
Maximillia C. Hottenrott ◽  
Eleni Stamellou ◽  
Annette Breedijk ◽  
Charalambos Tsagogiorgas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Transcription Factors ◽  
T Cell ◽  
Cell Cycle Arrest ◽  
T Cell Proliferation ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

SF1126, a Pan-PI3K Inhibitor Has Superior Preclinical Activity to CAL-101 a PI3K Delta-Specific Inhibitor in Aggressive B-Cell Non-Hodgkin's Lymphoma

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2720-2720 ◽  
Author(s):  
Daruka Mahadevan ◽  
Wenqing Qi ◽  
Amy Stejskal ◽  
Laurence Cooke ◽  
Joseph R Garlich
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
B Cell ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Specific Inhibitor ◽  
Pi3k Pathway ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

Abstract Abstract 2720 The PI3K pathway is constitutively active in B-cell non-Hodgkin lymphomas (B-NHL). PI3K pathway targeted therapies have focused on inhibiting mTORC1 (rapalogs) with a ∼20–48% response rate due to inactivation of mTORC1 resulting in G1 cell-cycle arrest or apoptosis. A mechanism of resistance to rapalogs is that mTORC2 is unaffected resulting in undesirable Akt activation. Strategies to block Akt up-regulation require novel agents that simultaneously block PI3K, mTORC1 and mTORC2. SF1126 is a novel pan-PI3K/mTORC1/mTORC2 inhibitor conjugated to an integrin targeted peptide RGD with potent anti-tumor activity in multiple solid tumor types. Here, we demonstrated SF1126 had potent anti-B-NHL activity and is superior to CAL-101 a PI3K delta-isoform specific inhibitor in a panel of aggressive B-NHL cell lines. Cells treated with SF1126 exhibited >90% decrease in pAkt and pGSK-3β confirming the mechanism of action of a pan-PI3K inhibitor. Moreover, SF1126 induced apoptosis in a dose and time dependent manner confirmed by flow cytometry, PARP cleavage and with an IC50 < 4μM. In contrast, CAL-101 was less active compared to SF1126 in inducing apoptosis (12% versus 25% in SUDHL-4 and 15% versus 23% in TMD-8) and cell proliferation (5.62μM versus 3.28μM SUDHL-4 and 5.31μM versus 1.47μM in TMD-8). SF1126 induced G1 cell cycle arrest at 2μM which contributes to suppression of cell proliferation. The cell cycle protein cyclin D1 is downstream of mTORC1, and the over-expression of cyclin D1 is a hallmark of mantle cell NHL (MCL). Consistent with this, cyclin D1 was significantly decreased by SF1126 compared to CAL-101. Lastly, the addition of Rituximab to SF1126 or CAL101 increased the apoptosis over single agent therapy in B-NHL cell lines. In conclusion, we demonstrate that SF1126 potently inhibits the constitutively activated PI3K/mTORC/Akt pathway in aggressive B-cell NHL cell lines with consequent suppressive effects on cell cycle progression, cell proliferation and induction of apoptosis. These findings provide a rationale for SF1126 in combination with rituximab as a novel therapeutic strategy for aggressive B-NHL and warrant early phase clinical trial evaluation [Funded by the Lymphoma SPORE 1 P50 CA 130805 01A1]. Disclosures: Garlich: Semafore Pharmaceuticals: Employment, Equity Ownership, Membership on an entity's Board of Directors or advisory committees, Patents & Royalties.

Anti-diabetic drug metformin inhibits cell proliferation and tumor growth in gallbladder cancer via G0/G1 cell cycle arrest

2020 ◽  
Vol 31 (3) ◽  
pp. 231-240 ◽  
Author(s):  
Takuma Yamashita ◽  
Kiyohito Kato ◽  
Shintaro Fujihara ◽  
Hisakazu Iwama ◽  
Asahiro Morishita ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Gallbladder Cancer ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest
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