Correction to Low Dose of Amino-Modified Nanoparticles Induces Cell Cycle Arrest

1537 Background: Clinical and preclinical studies suggest that cyclooxygenase (COX)-2 inhibitors reduce the risk of various cancers, however, their administration is associated with an increased cardiovascular risk. Agents with 5-LOX/COX inhibition provide a possible approach for improving chemopreventive efficacy without unwanted side effects. COX and LOX inhibition have also been associated with an increase in PPAR γ expression. The present experiments tested the effects of licofelone (L) in breast cancer cell lines and assessed whether dual inhibition of LOX and COX may potentiate the action of rosiglitazone (R). Methods: MDA-MB-231 and MCF-7 cells were exposed to sub-toxic concentrations of L and R alone and in combination and analyzed for growth inhibition (MTT method), apoptosis (EB-AO and DAPI methods), cell-cycle analysis (flow cytometry), and protein expression (immunoblot method). Results: L and R inhibited cell growth in a dose-dependent manner in both cell lines. Combination therapy resulted in significant rates of apoptosis, particularly at high doses in both cell lines (p<0.001). Flow cytometric analysis showed that L and R exhibited cell cycle arrest at the G0/G1 phase in MDA-MB-231 cells. The low dose combination did not promote cell cycle arrest while the higher dose combination therapy demonstrated significant inhibition (p <0.0009). In MCF-7 cells, G0/G1 phase blockade was noted in L and R treated cells as well as in the low dose simultaneous combination therapy. Intermediate and high dose combination therapy exhibited increased cell cycle arrest at G0/G1 when L was administered 12 hours before R (p = 0.0030 and 0.0017). Western blot analysis showed increased expression of p21WAFI/CIPI and decreased cyclin D1 expression in both cell lines after therapy. Both agents induced caspase-3 expression in MDA-MB-231 cells at high concentrations, with even higher expression observed in the combination treatment. MCF-7 cells demonstrated PARP cleavage at all doses when compared to control. Conclusions: Our results suggest that L is a potential agent for prevention and treatment of breast cancer and the combination of low doses of L and R provide further promise in improving efficacy against breast cancer. No significant financial relationships to disclose.

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Low-Dose Hyper-radiosensitivity: A Consequence of Ineffective Cell Cycle Arrest of Radiation-Damaged G2-Phase Cells

Radiation Research ◽

10.1667/rr3130 ◽

2004 ◽

Vol 161 (3) ◽

pp. 247-255 ◽

Cited By ~ 159

Author(s):

B. Marples ◽

B. G. Wouters ◽

S. J. Collis ◽

A. J. Chalmers ◽

M. C. Joiner

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Low Dose ◽

Cycle Arrest ◽

G2 Phase

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Dose Dependent Biological Effects of Idarubicin in HL-60 Cells: Alterations of the Cell-Cycle and Apoptosis

Acta Medica (Hradec Kralove Czech Republic) ◽

10.14712/18059694.2019.116 ◽

2000 ◽

Vol 43 (2) ◽

pp. 69-73 ◽

Cited By ~ 3

Author(s):

Martina Mareková ◽

Jiřina Vávrová ◽

Doris Vokurková

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Low Dose ◽

Biological Effects ◽

Cell Cycle Phase ◽

Cycle Phase ◽

Cycle Arrest ◽

Dose Dependent ◽

Massive Apoptosis ◽

Human Leukaemia

TP-53 deficient cells of human leukaemia HL-60 die by massive apoptosis after treatment by high (50-100 nmol/l) doses of DNA damaging agent Idarubicin, regardless of the cell-cycle phase, in which they are affected. In contrary, after relatively low dose 10 nmol/l the cells die after cell-cycle arrest in G2phase. The results show, that apoptosis induced by idarubicin could appear independently of the cell-cycle phase and that period in which apoptosis is observed is related to the dose of Idarubicin.

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Low Dose of Amino-Modified Nanoparticles Induces Cell Cycle Arrest

ACS Nano ◽

10.1021/nn403126e ◽

2013 ◽

Vol 7 (9) ◽

pp. 7483-7494 ◽

Cited By ~ 59

Author(s):

Jong Ah Kim ◽

Christoffer Åberg ◽

Guillermo de Cárcer ◽

Marcos Malumbres ◽

Anna Salvati ◽

...

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Low Dose ◽

Cycle Arrest

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Effect of Hsp90 Inhibitor KW-2478 on HepG2 Cells

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520619666191023094610 ◽

2020 ◽

Vol 19 (18) ◽

pp. 2231-2242 ◽

Cited By ~ 2

Author(s):

Xiaomin Chang ◽

Xuerong Zhao ◽

Jianping Wang ◽

Shi Ding ◽

Lijun Xiao ◽

...

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Hepg2 Cells ◽

Low Dose ◽

Quantitative Polymerase Chain Reaction ◽

Mrna Levels ◽

Related Factors ◽

Regulatory Pathways ◽

Cycle Arrest ◽

Induced Apoptosis

Objective: The objectives of this study were to investigate the effects of proliferation, apoptosis, cell cycle, invasion, and senescence of KW-2478 on HepG2 cells, and to explore the related mechanism of apoptosis and the cell cycle. Methods: HepG2 cells (hepatocellular carcinoma cells) were cultured with KW-2478, at different doses and for different times, in vitro. The MTT assay was used to detect the effect of KW-2478 on proliferation of HepG2 cells. Flow cytometry was used to determine the effects of KW-2478 on the cell cycle and apoptosis of HepG2 cells. The Transwell assay was used to determine the effect of KW-2478 on cell invasion. The β-galactosidase assay tested the effect of low-dose KW-2478 on the senescence of HepG2 cells. Western blotting and the quantitative polymerase chain reaction were used respectively to assess changes in protein and mRNA levels of related factors in HepG2 cells after the KW-2478 treatment. Results: KW-2478 significantly inhibited proliferation of HepG2 cells. KW-2478 induced apoptosis and cell cycle arrest of HepG2 cells, and inhibited the invasion of HepG2 cells; low dose KW-2478 promoted HepG2 senescence. Conclusions: KW-2478 inhibited the proliferation of HepG2 cells, induced apoptosis and cell cycle arrest, inhibited invasion, and promoted senescence. KW-2478 affected the expression of related factors in the mitochondrial apoptotic signaling and cell cycle-related regulatory pathways. KW-2478 downregulated the expression of STAT3, which is a key factor in the JAK-STAT pathway, indicating that KW-2478 may affect the function of HepG2 cells by downregulating STAT3.

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