Lithium Modulates Cancer Cell Growth, Apoptosis, Gene Expression and Cytokine Production in HL-60 Promyelocytic Leukaemia Cells and Their Drug-Resistant Sub-clones

2012 ◽  
Vol 149 (3) ◽  
pp. 323-330 ◽  
Author(s):  
Thabe Matsebatlela ◽  
Vincent Gallicchio ◽  
Rolf Becker
2011 ◽  
Vol 9 (5) ◽  
pp. 660-670 ◽  
Author(s):  
Chen-Yin Ou ◽  
Melissa J. LaBonte ◽  
Philipp C. Manegold ◽  
Alex Yick-Lun So ◽  
Irina Ianculescu ◽  
...  

2019 ◽  
Vol 234 (11) ◽  
pp. 20608-20622 ◽  
Author(s):  
William J. Wulftange ◽  
Michelle A. Rose ◽  
Marcial Garmendia‐Cedillos ◽  
Davi da Silva ◽  
Joanna E. Poprawski ◽  
...  

2014 ◽  
Vol 46 (5) ◽  
pp. 409-414 ◽  
Author(s):  
A. Huang ◽  
B. Bao ◽  
H. R. Gaskins ◽  
H. Liu ◽  
X. Zhang ◽  
...  

2007 ◽  
Vol 27 (13) ◽  
pp. 4968-4979 ◽  
Author(s):  
Dmitri Wiederschain ◽  
Lin Chen ◽  
Brett Johnson ◽  
Kimberly Bettano ◽  
Dowdy Jackson ◽  
...  

ABSTRACT Bmi-1 and Mel-18 are structural homologues that belong to the Polycomb group of transcriptional regulators and are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. While a number of clinical and experimental observations have implicated Bmi-1 in human tumorigenesis, the role of Mel-18 in cancer cell growth has not been investigated. We report here that short hairpin RNA-mediated knockdown of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival, anchorage-independent growth, and suppression of tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increases the clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone does not affect the growth of normal human WI38 fibroblasts. Proteomics-based characterization of Bmi-1 and Mel-18 protein complexes isolated from cancer cells revealed substantial similarities in their respective compositions. Finally, gene expression analysis identified a number of cancer-relevant pathways that may be controlled by Bmi-1 and Mel-18 and also showed that these Polycomb proteins regulate a set of common gene targets. Taken together, these results suggest that Bmi-1 and Mel-18 may have overlapping functions in cancer cell growth.


2011 ◽  
Vol 40 (4) ◽  
pp. 935-941 ◽  
Author(s):  
CARMINE SPAMPANATO ◽  
SALVATORE DE MARIA ◽  
MADDALENA SARNATARO ◽  
ELISABETTA GIORDANO ◽  
MARIO ZANFARDINO ◽  
...  

2021 ◽  
Vol 15 (1) ◽  
pp. 19
Author(s):  
Irmanida Batubara ◽  
Arif Rakhman Hakim ◽  
Silmi Mariya ◽  
Suminar Setiati Achmadi ◽  
Valentina Sokoastri Valentina Sokoastri ◽  
...  

Background: 9,10-Anthraquinone (9,10-AQ) is a contaminant on some agricultural products and considered as carcinogenic based on EU Regulation No. 1146/2014. Except for little evidence on experimental rats, there is no strong proof regarding the carcinogenicity in humans. Therefore, it is essential to find a safe dose of this compound since the difference in 9,10-AQ levels will affect cancer cell growth. This research aims to find the 9,10-AQ concentration that does not proliferate the human cancer cells under in vitro study.Methods: In determining the 9,10-AQ concentration that does not proliferate the cancer cells growth, 0.01 to 500 mg/L 9,10-AQ was directly tested on four human cancer cells (colorectal carcinoma HCT 116, colon adenocarcinoma WiDr, breast cancer MCF-7, and cervical cancer HeLa), and the viability of the cells was counted via (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay. In the gene expression level, the effects on a selected cancer cell line were determined by qRT-PCR against BAX, BCL-2, PCNA, and P53.Results: The result indicates that 9,10-AQ up to 500 mg/L concentration does not proliferate the cell’s growth but instead inhibits those four cancer cells’ growths. The concentration of 9,10-AQ that inhibits 50% the cancer cells growth (IC50) value was 321.8 mg/L (1.55 mM) against HCT 116 and above 500 mg/L (above 2.40 mM) against WiDr, MCF-7, and HeLa. The 9,10-AQ at 500 mg/L (or 2.40 mM) increases BAX expression and acts as an apoptotic agent on HeLa cells.Conclusions: The investigation has shown that 9,10-AQ up to 500 mg/L concentration does not proliferate the cancer cell growth; instead, it inhibits the HCT 116 and HeLa cells growth. We have preliminary evidence regarding the apoptotic mechanism of 9,10-AQ by increasing BAX gene expression on HeLa cells.


2005 ◽  
Vol 288 (3) ◽  
pp. G447-G456 ◽  
Author(s):  
Anping Chen ◽  
Jianye Xu

Colorectal cancer is a leading cause of cancer-related morbidity and mortality in the United States. Curcumin, the yellow pigment in turmeric, possesses inhibitory effects on growth of a variety of tumor cells by reducing cell proliferation and inducing apoptosis. Effects of the peroxisome proliferator-activated receptor-γ (PPARγ) on stimulating cell differentiation and on inducing cell cycle arrest have attracted attention from the perspective of treatment and prevention of cancer. The aim of this study was to elucidate the mechanisms by which curcumin inhibits colon cancer cell growth. In the present report, we observed that curcumin, in a dose-dependent manner, inhibited the growth of Moser cells, a human colon cancer-derived cell line, and stimulated the trans-activating activity of PPARγ. Further studies demonstrated that activation of PPARγ was required for curcumin to inhibit Moser cell growth. Activation of PPARγ mediated curcumin suppression of the expression of cyclin D1, a critical protein in the cell cycle, in Moser cells. In addition, curcumin blocked EGF signaling by inhibiting EGF receptor (EGFR) tyrosine phosphorylation and suppressing the gene expression of EGFR mediated by activation of PPARγ. In addition to curcumin reduction of the level of phosphorylated PPARγ, inhibition of cyclin D1 expression played a major and significant role in curcumin stimulation of PPARγ activity in Moser cells. Taken together, our results demonstrated for the first time that curcumin activation of PPARγ inhibited Moser cell growth and mediated the suppression of the gene expression of cyclin D1 and EGFR. These results provided a novel insight into the roles and mechanisms of curcumin in inhibition of colon cancer cell growth and potential therapeutic strategies for treatment of colon cancer.


2006 ◽  
Vol 175 (4S) ◽  
pp. 257-257
Author(s):  
Jennifer Sung ◽  
Qinghua Xia ◽  
Wasim Chowdhury ◽  
Shabana Shabbeer ◽  
Michael Carducci ◽  
...  

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