scholarly journals The negative interplay between Aurora A/B and BRCA1/2 controls cancer cell growth and tumorigenesis via distinct regulation of cell cycle progression, cytokinesis, and tetraploidy

2014 ◽  
Vol 13 (1) ◽  
pp. 94 ◽  
Author(s):  
Yan Wang ◽  
Ziliang Wang ◽  
Zihao Qi ◽  
Sheng Yin ◽  
Na Zhang ◽  
...  
Medicine ◽  
2014 ◽  
Vol 93 (28) ◽  
pp. e294 ◽  
Author(s):  
Kaiwu Xu ◽  
Xinming Song ◽  
Zhihui Chen ◽  
Changjiang Qin ◽  
Yulong He ◽  
...  

2015 ◽  
pp. 4631 ◽  
Author(s):  
Kun-Chun Chiang ◽  
Chun-Nan Yeh ◽  
Huang-Yang Chen ◽  
Jong-Hwei S.Pang ◽  
Shang-Yu Wang ◽  
...  

2019 ◽  
Vol 9 (4) ◽  
pp. 685-689 ◽  
Author(s):  
Andrea Rasmussen ◽  
Kaylee Murphy ◽  
David W. Hoskin

Purpose: Gingerol homologs found in the rhizomes of ginger plants have the potential to benefithuman health, including the prevention and treatment of cancer. This study evaluated the effectof 10-gingerol on ovarian cancer cell (HEY, OVCAR3, and SKOV-3) growth.Methods: Cell growth was measured by MTT assays, flow cytometry was used to assess cellproliferation, cytotoxicity and cell cycle progression, and western blotting was used to measurecyclin protein expression.Results: Ovarian cancer cells that were treated with 10-gingerol experienced a time- anddose-dependent decrease in cell number, which was due to a reduction in cell proliferationrather than a cytotoxic effect. Reduced proliferation of 10-gingerol-treated ovarian cancercells was associated with an increased percentage of cells in G2 phase of the cell cycle anda corresponding reduction in the percentage of cells in G1. Ovarian cancer cells also showeddecreased cyclin A, B1, and D3 expression following exposure to 10-gingerol.Conclusion: These findings revealed that 10-gingerol caused a G2 arrest-associated suppressionof ovarian cancer cell growth, which may be exploited in the management of ovarian cancer.<br />


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Yantao Li ◽  
Jiajun Huang ◽  
Wanjun Lin ◽  
Zhongwen Yuan ◽  
Senling Feng ◽  
...  

Gynostemma pentaphyllum(Thunb.) Makino (GpM) has been widely used in traditional Chinese medicine (TCM) for the treatment of various diseases including cancer. Most previous studies have focused primarily on polar fractions of GpM for anticancer activities. In this study, a nonpolar fraction EA1.3A from GpM showed potent growth inhibitory activities against four cancer cell lines with IC50ranging from 31.62 μg/mL to 38.02 μg/mL. Furthermore, EA1.3A also inhibited the growth of breast cancer cell MDA-MB-453 time-dependently, as well as its colony formation ability. EA1.3A induced apoptosis on MDA-MB-453 cells both dose-dependently and time-dependently as analyzed by flow cytometry and verified by western blotting analysis of apoptosis marker cleaved nuclear poly(ADP-ribose) polymerase (cPARP). Additionally, EA1.3A induced cell cycle arrest in G0/G1 phase. Chemical components analysis of EA1.3A by GC-MS revealed that this nonpolar fraction from GpM contains 10 compounds including four alkaloids, three organic esters, two terpenes, and one catechol substance, and all these compounds have not been reported in GpM. In summary, the nonpolar fraction EA1.3A from GpM inhibited cancer cell growth through induction of apoptosis and regulation of cell cycle progression. Our study shed light on new chemical bases for the anticancer activities of GpM and feasibilities to develop new anticancer agents from this widely used medicinal plant.


2019 ◽  
Vol 26 (11) ◽  
pp. 800-818
Author(s):  
Zujian Xiong ◽  
Xuejun Li ◽  
Qi Yang

Pituitary Tumor Transforming Gene (PTTG) of human is known as a checkpoint gene in the middle and late stages of mitosis, and is also a proto-oncogene that promotes cell cycle progression. In the nucleus, PTTG works as securin in controlling the mid-term segregation of sister chromatids. Overexpression of PTTG, entering the nucleus with the help of PBF in pituitary adenomas, participates in the regulation of cell cycle, interferes with DNA repair, induces genetic instability, transactivates FGF-2 and VEGF and promotes angiogenesis and tumor invasion. Simultaneously, overexpression of PTTG induces tumor cell senescence through the DNA damage pathway, making pituitary adenoma possessing the potential self-limiting ability. To elucidate the mechanism of PTTG in the regulation of pituitary adenomas, we focus on both the positive and negative function of PTTG and find out key factors interacted with PTTG in pituitary adenomas. Furthermore, we discuss other possible mechanisms correlate with PTTG in pituitary adenoma initiation and development and the potential value of PTTG in clinical treatment.


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