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

2000 ◽  
Vol 43 (2) ◽  
pp. 69-73 ◽  
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.

SMBA1, a Bax Activator, Induces Cell Cycle Arrest and Apoptosis in Malignant Glioma Cells

Pharmacology ◽  
2019 ◽  
Vol 105 (3-4) ◽  
pp. 164-172
Author(s):  
Shuangbo Fan ◽  
Qian Xu ◽  
Liang Wang ◽  
Yulin Wan ◽  
Sheng Qiu
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Biological Effects ◽  
Cyclin B1 ◽  
Dependent Manner ◽  
Apoptosis Pathway ◽  
Cycle Arrest ◽  
Intrinsic Apoptosis Pathway ◽  
Induced Apoptosis ◽  
Dose Dependent

SMBA1 (small-molecule Bax agonists 1), a small molecular activator of Bax, is a potential anti-tumour agent. In the present study, we investigated the biological effects of SMBA1 on glioblastoma (GBM) cells. SMBA1 reduced the viabilities of U87MG, U251 and T98G cells in a time- and dose-dependent manner. Moreover, treatment with SMBA1 induced cell cycle arrest at the G2/M phase transition, accompanied by the downregulation of Cdc25c and cyclin B1 and the upregulation of p21. SMBA1 also induced apoptosis of GBM cells in a dose-dependent manner. Mechanistically, SMBA1 induced apoptosis via the intrinsic pathway. Silencing of Bax or ectopic expression of Bcl-2 significantly inhibited SMBA1-induced apoptosis. Moreover, SMBA1 inhibited the growth of U87MG xenograft tumours in vivo. Overall, SMBA1 shows anti-proliferative effects against GBM cells through activation of the intrinsic apoptosis pathway.

scholarly journals Image-Based Detection of Patient-Specific Drug-Induced Cell-Cycle Effects in Glioblastoma

2018 ◽  
Vol 23 (10) ◽  
pp. 1030-1039
Author(s):  
Damian J. Matuszewski ◽  
Carolina Wählby ◽  
Cecilia Krona ◽  
Sven Nelander ◽  
Ida-Maria Sintorn
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Dna Content ◽  
Nuclear Dna ◽  
Nuclear Dna Content ◽  
Cell Cycle Phase ◽  
Patient Specific ◽  
Cycle Phase ◽  
Glioblastoma Cells ◽  
Cycle Arrest

Image-based analysis is an increasingly important tool to characterize the effect of drugs in large-scale chemical screens. Herein, we present image and data analysis methods to investigate population cell-cycle dynamics in patient-derived brain tumor cells. Images of glioblastoma cells grown in multiwell plates were used to extract per-cell descriptors, including nuclear DNA content. We reduced the DNA content data from per-cell descriptors to per-well frequency distributions, which were used to identify compounds affecting cell-cycle phase distribution. We analyzed cells from 15 patient cases representing multiple subtypes of glioblastoma and searched for clusters of cell-cycle phase distributions characterizing similarities in response to 249 compounds at 11 doses. We show that this approach applied in a blind analysis with unlabeled substances identified drugs that are commonly used for treating solid tumors as well as other compounds that are well known for inducing cell-cycle arrest. Redistribution of nuclear DNA content signals is thus a robust metric of cell-cycle arrest in patient-derived glioblastoma cells.

Molecular Mechanisms of Thymoquinone as Anticancer agent

2020 ◽  
Vol 23 ◽  
Author(s):  
Fatma Ismail Alhmied ◽  
Ali Hassan Alammar ◽  
Bayan Mohammed Alsultan ◽  
Marooj Alshehri ◽  
Faheem Hyder Pottoo
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Human Breast Cancer ◽  
Phase Cell ◽  
Cycle Phase ◽  
Human Breast ◽  
Cycle Arrest ◽  
Phase Arrest ◽  
Anti Cancer

Abstract:: Thymoquinone (TQ), the bioactive constituent of Nigella Sativa seeds is a well-known natural compound for the management of several types of cancers. The anti-cancer properties of thymoquinone are thought to be operated via intervening with various oncogenic pathways including cell cycle arrest, prevention of inflammation and oxidative stress, induction of invasion, metastasis, inhibition of angiogenesis, and apoptosis. As well as up-regulation and down-regulation of specific tumor suppressor genes and tumor promoting genes, respectively. Proliferation of various tumor cells is inhibited by TQ via induction of cell cycle arrest, disruption of the microtubule organization, and down regulating cell survival protein expression. TQ induces G1 phase cell cycle arrest in human breast cancer, colon cancer and osteosarcoma cells through inhibiting the activation of cyclin E or cyclin D and up-regulating p27and p21 a cyclin dependent kinase (Cdk) inhibitor. TQ concentration is a significant factor in targeting a particular cell cycle phase. While high concentration of TQ induced G2 phase arrest in human breast cancer (MCF-7) cells, low concentration causes S phase arrest. This review article provides mechanistic insights into the anti-cancer properties of thymoquinone.

scholarly journals Alantolactone pyrazoline analogue inhibits cancer cell proliferation and induces apoptosis in non-small cell lung carcinoma cells

2015 ◽  
Vol 10 (2) ◽  
pp. 409 ◽  
Author(s):  
Jing Lv ◽  
Ming-Qin Cao ◽  
Jian-Chun Yu
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Cycle Arrest ◽  
Chromatin Condensation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Cycle Arrest ◽  
H460 Cells ◽  
Dose Dependent

<p>The aim of the current study was to evaluate the anticancer and apoptotic effects of alantolactone pyrazoline analogue in human non-small cell lung cancer (NCI-H460) cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zolium bromide) assay was used to evaluate the cell viability while as fluorescence microscopy was used to assess the effect on apoptosis, cellular and nuclear morphology. Flow cytometry evaluated the effect of APA on cell cycle arrest in these cells. The results revealed that APA induced potent, time and dose-dependent cytotoxic effects on the growth of NCI-H460 cells. It also inhibited colony forming tendency as well as cell invasion capability of these cancer cells. APA induced dose-dependent nuclear and cellular morphological effects including chromatin condensation and DNA fragmentation. Flow cytometry revealed that the anticancer effects of APA might be due to its cell cycle arrest inducing tendency in G0/G1 phase of the cell cycle.</p>

Silencing of miR-1246 Induces Cell Cycle Arrest and Apoptosis in Cisplatin-Resistant Ovarian Cancer Cells by Promoting ZNF23 Transcription

2021 ◽  
pp. 1-13
Author(s):  
Lu Cai ◽  
Qian Zhang ◽  
Lili Du ◽  
Feiyun Zheng
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cell Cycle Progression ◽  
Luciferase Reporter ◽  
Cycle Phase ◽  
Ovarian Cancer Cells ◽  
Tunel Staining ◽  
Cycle Arrest

Ovarian cancer (OC) is the most frequent cause of death among patients with gynecologic malignancies. In recent years, the development of cisplatin (DDP) resistance has become an important reason for the poor prognosis of OC patients. Therefore, it is vital to explore the mechanism of DDP resistance in OC. In this study, microRNA-1246 (miR-1246) expression in OC and DDP-resistant OC cells was determined by RT-qPCR, and chemosensitivity to DDP was assessed by the CCK-8 assay. A dual-luciferase reporter assay was performed to confirm the interaction between miR-1246 and zinc finger 23 (<i>ZNF23</i>), while changes in <i>ZNF23</i> expression were monitored by RT-qPCR, immunofluorescence, and western blot assays. Moreover, cell proliferation, cycle phase, and apoptosis were determined by EdU staining, flow cytometry, TUNEL staining, and Hoechst staining. Our data showed that miR-1246 was highly expressed in DDP-resistant OVCAR-3 and TOV-112D cells. Functionally, overexpression of miR-1246 markedly enhanced DDP resistance and cell proliferation, and suppressed cell cycle arrest and apoptosis of OC cells. Inhibition of miR-1246 expression significantly attenuated DDP resistance and cell proliferation, and increased cell cycle arrest and apoptosis in DDP-resistant OC cells. Furthermore, <i>ZNF23</i> was identified as a target gene of miR-1246, and ZNF23 protein expression was notably downregulated in DDP-resistant OC cells. Moreover, overexpression of miR-1246 significantly downregulated the <i>ZNF23</i> levels in OVCAR-3 and TOV-112D cells, and inhibition of miR-1246 upregulated the <i>ZNF23</i> levels in the DDP-resistant OVCAR-3 and TOV-112D cells. In conclusion, miR-1246 might be a novel regulator of DDP-resistant OC that functions by regulating <i>ZNF23</i> expression in DDP-resistant cells, as well as cell proliferation, cell cycle progression, and apoptosis.

scholarly journals The N-Terminal 24 Amino Acids of the p55 Gamma Regulatory Subunit of Phosphoinositide 3-Kinase Binds Rb and Induces Cell Cycle Arrest

2003 ◽  
Vol 23 (5) ◽  
pp. 1717-1725 ◽  
Author(s):  
Xianmin Xia ◽  
Aiwu Cheng ◽  
Damilola Akinmade ◽  
Anne W. Hamburger
Keyword(s):  
Cell Cycle ◽  
Amino Acid ◽  
Cell Cycle Arrest ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Biological Effects ◽  
Cycle Progression ◽  
Regulatory Subunits ◽  
Cycle Arrest ◽  
Phosphoinositide 3 Kinase

ABSTRACT Although phosphoinositide 3-kinase (PI 3-kinase) is essential for cell cycle progression, the molecular mechanisms that regulate its diverse biological effects are poorly understood. We demonstrate here that Rb, a key regulator of cell cycle progression, associates with p55 kDa (p55α and p55γ) regulatory subunits of PI 3-kinase in vivo and in vitro. Both confocal microscopy and biochemical analysis demonstrated the presence of p55γ in the nucleus. The 24-amino-acid N-terminal end of p55γ, which is unique among PI 3-kinase regulatory subunits, was sufficient to bind Rb. Addition of serum or growth factors to quiescent cells triggered the dissociation of Rb from p55. Ectopic expression of the 24-amino-acid N-terminal end of p55γ inhibited cell cycle progression, as evidenced by induction of cell growth arrest at the G0/G1 phase, inhibition of DNA synthesis, inhibition of cyclin D and cyclin E promoter activity, and changes in the expression of cell cycle-related proteins. The inhibitory effects of the N-terminal end of p55γ on cell cycle progression depended on the presence of functional Rb. These data demonstrate for the first time an association of p55γ with Rb and show that modification of this association can lead to cell cycle arrest.

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

ACS Nano ◽  
2013 ◽  
Vol 7 (11) ◽  
pp. 10433-10433 ◽  
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

scholarly journals Comparison of Two Components of Propolis: Caffeic Acid (CA) and Caffeic Acid Phenethyl Ester (CAPE) to Induce Apoptosis and Cell Cycle Arrest of Breast Cancer Cells MDA-MB-231

2017 ◽  
Author(s):  
Agata Kabała-Dzik ◽  
Anna Rzepecka-Stojko ◽  
Robert Kubina ◽  
Żaneta Jastrzębska-Stojko ◽  
Rafał Stojko ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Caffeic Acid ◽  
Annexin V ◽  
Caffeic Acid Phenethyl Ester ◽  
Dead Cell ◽  
Cycle Arrest ◽  
Ic50 Values ◽  
Dose Dependent

1) Background: Studies indicate that caffeic acid (CA), caffeic acid phenethyl ester (CAPE) are compounds with potent chemopreventive effects. Breast cancer is a common cancer among women worldwide. The study shows comparison of caffeic acid and its ester activity in the cells of breast cancer line MDA-MB-231; 2) Methods: The cells of MDA-MB-231 were treated by CA and CAPE with doses from 10 to 100 µM in time 24 h and 48 h. Cytotoxicity MTT test, apoptosis by Annexin V and cell cycle with Dead Cell Assay were performed; 3) Results: The cytotoxic activity was greater for CAPE comparing to CA, in both incubation time (same dosage). IC50 values for CAPE were 27.84 (24h) and 15.83 (48h) and &gt;10000 (24h) and &gt;1000 (48h) for CA. Polyphenols induced apoptosis, higher apoptotic effect observed for CAPE (dose dependent). CAPE induced cell cycle arrest in S phase (time and dose dependent). Dose dependent decline G0/G1 phase (48h) and elimination of phase G2/M (100 µM of CAPE). For CA, only after 48 hours, small effect of cell cycle at phase S (however dose dependent), and slight decline of phase G0/G1 and G2/M only for highest doses (50 and 100 µM); 4) Conclusions: Comparing CA and CAPE activity, on the MDA-MB-231, we clearly see better activity of CAPE, with the same dosage and experiment time.

scholarly journals Pinocembrin flavanone inhibits cell viability in PC-3 human prostate cancer by inducing cellular apoptosis, ROS production and cell cycle arrest

2021 ◽  
Vol 71 (4) ◽  
pp. 669-678
Author(s):  
Linhai Shao ◽  
Yajun Shao ◽  
Yu Yuan
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Human Prostate ◽  
Ros Production ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Dose Dependent

Abstract The main purpose of the present study was to evaluate the antitumor effects of pinocembrin in human prostate cancer cells (PC-3) along with investigating its effects on cell apoptosis, endogenous ROS production and cell cycle. MTT assay and clonogenic assays were used to study the effects on cell viability and cancer colony formation, respectively. Fluorescence microscopy along with Western blotting was used to study apoptotic effects induced by pinocembrin. Flow cytometry was used to study effects on ROS production and cell cycle phase distribution. Results indicated that pinocembrin promoted inhibition cell proliferation along with reducing cancer colony formation of PC-3 cells in a dose-dependent manner. Pinocembrin induced regulatory effects over expressions of caspase-3, caspase-9, Bax and Bcl-2, thereby promoting apoptotic cell death in PC-3 cells. It also led to the dose-dependent G0/G1 cell cycle arrest. In conclusion, pinocembrin exhibits strong anticancer effects in human prostate cancer cells mediated via apoptosis, endogenous ROS production and G0/G1 cell cycle arrest.

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