Induction of G1 cell cycle arrest and cyclin D1 down-regulation in response to pericarp extract of Baneh in human breast cancer T47D cells

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.

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Cytotoxic Activity, Apoptosis Induction and Cell Cycle Arrest in Human Breast Cancer (MCF7) Cells by a Novel Fluorinated Tetrahydro-[1,2,4]Triazolo[3,4-a]Isoquinolin Chalcones

Polycyclic Aromatic Compounds ◽

10.1080/10406638.2021.2014535 ◽

2021 ◽

pp. 1-20

Author(s):

Magda F. Mohamed ◽

Nada S. Ibrahim ◽

Sherif Abdelaziz Ibrahim ◽

May A. El-Manawaty ◽

Salwa M. El-Hallouty ◽

...

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Cytotoxic Activity ◽

Cell Cycle Arrest ◽

Human Breast Cancer ◽

Apoptosis Induction ◽

Human Breast ◽

Mcf7 Cells ◽

Cycle Arrest

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Globularifolin inhibits CAMA-1 human breast cancer cell line via cell cycle arrest, apoptosis and inhibition of PI3K/AKT signalling pathway

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v17i9.4 ◽

2018 ◽

Vol 17 (9) ◽

pp. 1711

Author(s):

Yu Chen ◽

Zhenwu Wang ◽

Mei Liu ◽

Xiaodong Wang ◽

Linghan Zhang ◽

...

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Cell Cycle Arrest ◽

Cell Line ◽

Breast Cancer Cell Line ◽

Human Breast Cancer ◽

Cancer Cell Line ◽

Human Breast Cancer Cell ◽

Human Breast ◽

Cycle Arrest

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Everolimus induces G1 cell cycle arrest through autophagy-mediated protein degradation of cyclin D1 in breast cancer cells

AJP Cell Physiology ◽

10.1152/ajpcell.00390.2018 ◽

2019 ◽

Vol 317 (2) ◽

pp. C244-C252 ◽

Cited By ~ 7

Author(s):

Guang Chen ◽

Xiao-Fei Ding ◽

Hakim Bouamar ◽

Kyle Pressley ◽

Lu-Zhe Sun

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Cyclin D1 ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Breast Tissue ◽

Human Breast ◽

Human Breast Tissue ◽

Cycle Arrest

Everolimus inhibits mammalian target of rapamycin complex 1 (mTORC1) and is known to cause induction of autophagy and G1 cell cycle arrest. However, it remains unknown whether everolimus-induced autophagy plays a critical role in its regulation of the cell cycle. We, for the first time, suggested that everolimus could stimulate autophagy-mediated cyclin D1 degradation in breast cancer cells. Everolimus-induced cyclin D1 degradation through the autophagy pathway was investigated in MCF-10DCIS.COM and MCF-7 cell lines upon autophagy inhibitor treatment using Western blot assay. Everolimus-stimulated autophagy and decrease in cyclin D1 were also tested in explant human breast tissue. Inhibiting mTORC1 with everolimus rapidly increased cyclin D1 degradation, whereas 3-methyladenine, chloroquine, and bafilomycin A1, the classic autophagy inhibitors, could attenuate everolimus-induced cyclin D1 degradation. Similarly, knockdown of autophagy-related 7 (Atg-7) also repressed everolimus-triggered cyclin D1 degradation. In addition, everolimus-induced autophagy occurred earlier than everolimus-induced G1 arrest, and blockade of autophagy attenuated everolimus-induced G1 arrest. We also found that everolimus stimulated autophagy and decreased cyclin D1 levels in explant human breast tissue. These data support the conclusion that the autophagy induced by everolimus in human mammary epithelial cells appears to cause cyclin D1 degradation resulting in G1 cell cycle arrest. Our findings contribute to our knowledge of the interplay between autophagy and cell cycle regulation mediated by mTORC1 signaling and cyclin D1 regulation.

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Ganoderma lucidum Extract Induces G1 Cell Cycle Arrest, and Apoptosis in Human Breast Cancer Cells

The American Journal of Chinese Medicine ◽

10.1142/s0192415x12500474 ◽

2012 ◽

Vol 40 (03) ◽

pp. 631-642 ◽

Cited By ~ 34

Author(s):

Guosheng Wu ◽

Zhengming Qian ◽

Jiajie Guo ◽

Dejun Hu ◽

Jiaolin Bao ◽

...

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Cancer Cells ◽

Human Breast Cancer ◽

Breast Cancer Cells ◽

Human Breast Cancer Cells ◽

Human Breast ◽

Cycle Arrest ◽

G1 Cell Cycle Arrest ◽

Mcf 7

Ganoderma lucidum (Fr.) Karst is a traditional Chinese herb that has been widely used for centuries to treat various diseases including cancer. Herein, an ethanol-soluble and acidic component (ESAC), which mainly contains triterpenes, was prepared from G. lucidum and its anti-tumor effects in vitro were tested on human breast cancer cells. Our results showed that ESAC reduced the cell viability of MCF-7 and MDA-MB-231 cells in a concentration-dependent manner with IC50 of about 100 μg/mL and 60 μg/mL, respectively. DNA damage was detected by Comet assay and the increased expression of γ-H2AX after ESAC treatment was determined in MCF-7 cells. Moreover, ESAC effectively mediated G1 cell cycle arrest in both concentration- and time-dependent manners and induced apoptosis as determined by Hoechst staining, DNA fragment assay and Western blot analysis in MCF-7 cells. In conclusion, ESAC exerts anti-proliferation effects by inducing DNA damage, G1 cell cycle arrest and apoptosis in human breast cancer cells.

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