scholarly journals Moderate levels of dietary arachidonic acid reduced lipid accumulation and tended to inhibit cell cycle progression in the liver of Japanese seabass Lateolabrax japonicus

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Houguo Xu ◽  
Chengqiang Wang ◽  
Yuanqin Zhang ◽  
Yuliang Wei ◽  
Mengqing Liang
Author(s):  
Hongyou Zhao ◽  
Bin Yi ◽  
Zhipin Liang ◽  
Ches’Nique Phillips ◽  
Hui-Yi Lin ◽  
...  

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
André L. S. Cruz ◽  
Nina Carrossini ◽  
Leonardo K. Teixeira ◽  
Luis F. Ribeiro-Pinto ◽  
Patricia T. Bozza ◽  
...  

ABSTRACTIntracellular lipid accumulation has been associated with a poor prognosis in cancer. We have previously reported the involvement of lipid droplets in cell proliferation in colon cancer cells, suggesting a role for these organelles in cancer development. In this study, we evaluate the role of lipid droplets in cell cycle regulation and cellular transformation. Cell cycle synchronization of NIH 3T3 cells revealed increased numbers and dispersed distribution of lipid droplets specifically during S phase. Also, the transformed cell lineage NIH 3T3-H-rasV12showed an accumulation of both lipid droplets and PLIN2 protein above the levels in NIH 3T3 cells.PLIN2gene overexpression, however, was not able to induce NIH 3T3 cell transformation, disproving the hypothesis thatPLIN2is an oncogene. Furthermore, positive PLIN2 staining was strongly associated with highly proliferative Ki-67-positive areas in human colon adenocarcinoma tissue samples. Taken together, these results indicate that cell cycle progression is associated with tight regulation of lipid droplets, a process that is altered in transformed cells, suggesting the existence of a mechanism that connects cell cycle progression and cell proliferation with lipid accumulation.


2003 ◽  
Vol 474 (2-3) ◽  
pp. 185-193 ◽  
Author(s):  
Mark J. Belsey ◽  
Steven J. Culliford ◽  
Richard M. Morley ◽  
Harry J. Witchel ◽  
Roland Z. Kozlowski

Genetics ◽  
1998 ◽  
Vol 148 (2) ◽  
pp. 599-610
Author(s):  
Eric J Schott ◽  
M Andrew Hoyt

Abstract We identified an allele of Saccharomyces cerevisiae CDC20 that exhibits a spindle-assembly checkpoint defect. Previous studies indicated that loss of CDC20 function caused cell cycle arrest prior to the onset of anaphase. In contrast, CDC20-50 caused inappropriate cell cycle progression through M phase in the absence of mitotic spindle function. This effect of CDC20-50 was dominant over wild type and was eliminated by a second mutation causing loss of function, suggesting that it encodes an overactive form of Cdc20p. Overexpression of CDC20 was found to cause a similar checkpoint defect, causing bypass of the preanaphase arrest produced by either microtubule-depolymerizing compounds or MPS1 overexpression. CDC20 overexpression was also able to overcome the anaphase delay caused by high levels of the anaphase inhibitor Pds1p, but not a mutant form immune to anaphase-promoting complex- (APC-)mediated proteolysis. CDC20 overexpression was unable to promote anaphase in cells deficient in APC function. These findings suggest that Cdc20p is a limiting factor that promotes anaphase entry by antagonizing Pds1p. Cdc20p may promote the APC-dependent proteolytic degradation of Pds1p and other factors that act to inhibit cell cycle progression through mitosis.


2003 ◽  
Vol 18 (1) ◽  
pp. 146-148 ◽  
Author(s):  
Michaela Artwohl ◽  
Michael Roden ◽  
Werner Waldhäusl ◽  
Angelika Freudenthaler ◽  
Sabina M. Baumgartner‐Parzer

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