scholarly journals HMGB2 orchestrates the chromatin landscape of senescence-associated secretory phenotype gene loci

2016 ◽  
Vol 215 (3) ◽  
pp. 325-334 ◽  
Author(s):  
Katherine M. Aird ◽  
Osamu Iwasaki ◽  
Andrew V. Kossenkov ◽  
Hideki Tanizawa ◽  
Nail Fatkhutdinov ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Growth ◽  
Cellular Senescence ◽  
Growth Arrest ◽  
High Mobility ◽  
Cell Growth Arrest ◽  
Cytokines And Chemokines ◽  
Secreted Factors ◽  
Genes Encoding ◽  
Secretory Phenotype

Cellular senescence is a stable cell growth arrest that is characterized by the silencing of proliferation-promoting genes through compaction of chromosomes into senescence-associated heterochromatin foci (SAHF). Paradoxically, senescence is also accompanied by increased transcription of certain genes encoding for secreted factors such as cytokines and chemokines, known as the senescence-associated secretory phenotype (SASP). How SASP genes are excluded from SAHF-mediated global gene silencing remains unclear. In this study, we report that high mobility group box 2 (HMGB2) orchestrates the chromatin landscape of SASP gene loci. HMGB2 preferentially localizes to SASP gene loci during senescence. Loss of HMGB2 during senescence blunts SASP gene expression by allowing for spreading of repressive heterochromatin into SASP gene loci. This correlates with incorporation of SASP gene loci into SAHF. Our results establish HMGB2 as a novel master regulator that orchestrates SASP through prevention of heterochromatin spreading to allow for exclusion of SASP gene loci from a global heterochromatin environment during senescence.

Inducing cell growth arrest and apoptosis by silencing long non-coding RNA PCAT-1 in human bladder cancer

Tumor Biology ◽  
2015 ◽  
Vol 36 (10) ◽  
pp. 7685-7689 ◽  
Author(s):  
Li Liu ◽  
Yuchen Liu ◽  
Chengle Zhuang ◽  
Wen Xu ◽  
Xing Fu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Growth Arrest ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Cell Growth Arrest ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Lipid biomarkers of glioma cell growth arrest and cell death detected by 1 H magic angle spinning MRS

2012 ◽  
Vol 25 (11) ◽  
pp. 1253-1262 ◽  
Author(s):  
Ladan Mirbahai ◽  
Martin Wilson ◽  
Christopher S. Shaw ◽  
Carmel McConville ◽  
Roger D. G. Malcomson ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Glioma Cell ◽  
Growth Arrest ◽  
Magic Angle Spinning ◽  
Lipid Biomarkers ◽  
Magic Angle ◽  
Cell Growth Arrest ◽  
Angle Spinning

Cr (VI) induces cell growth arrest through hydrogen peroxide-mediated reactions

2001 ◽  
pp. 77-83
Author(s):  
Zhuo Zhang ◽  
Stephen S. Leonard ◽  
Suwei Wang ◽  
Val Vallyathan ◽  
Vince Castranova ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Growth ◽  
Growth Arrest ◽  
Cell Growth Arrest

scholarly journals Prevention of Cell Growth by Suppression of Villin Expression in Lithocholic Acid-Stimulated HepG2 Cells

2018 ◽  
Vol 67 (2) ◽  
pp. 129-141 ◽  
Author(s):  
Munetaka Ozeki ◽  
Wulamujiang Aini ◽  
Aya Miyagawa-Hayashino ◽  
Keiji Tamaki
Keyword(s):  
Cell Growth ◽  
Hepg2 Cells ◽  
Lithocholic Acid ◽  
Morphological Changes ◽  
Growth Arrest ◽  
Pregnane X Receptor ◽  
Farnesoid X Receptor ◽  
Bile Canaliculi ◽  
Cell Growth Arrest ◽  
Depth Analysis

Summary Cholestasis is a condition wherein bile flow is interrupted and lithocholic acid is known to play a key role in causing severe liver injury. In this study, we performed in-depth analysis of the morphological changes in bile canaliculi and the biological role of villin in cholestasis using lithocholic acid-stimulated HepG2 human hepatocarcinoma cells. We confirmed disruption of the bile canaliculi in liver sections from a liver allograft patient with cholestasis. Lithocholic acid caused strong cytotoxicity in HepG2 cells, which was associated with abnormal morphology. Lithocholic acid reduced villin expression, which recovered in the presence of nuclear receptor agonists. Furthermore, villin mRNA expression increased following small interfering RNA (siRNA)-mediated knockdown of the nuclear farnesoid X receptor and pregnane X receptor. Villin knockdown using siRNA caused cell growth arrest in HepG2 cells. The effect of villin-knockdown on whole-genome expression in HepG2 cells was analyzed by DNA microarray. Our data suggest that lithocholic acid caused cell growth arrest by suppressing villin expression via farnesoid X receptor and pregnane X receptor in HepG2 cells.

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