scholarly journals Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction

2021 ◽  
Vol 9 (12) ◽  
pp. 2594
Author(s):  
Chun-Yi Lin ◽  
Sanya Hamini ◽  
Peter Robert Tupa ◽  
Hisako Masuda
Keyword(s):  
Cell Growth ◽  
Ectopic Expression ◽  
Growth Arrest ◽  
Bacterial Genomes ◽  
Cellular Memory ◽  
Cell Growth Arrest ◽  
Growth Environment ◽  
The Past ◽  
Toxin Protein ◽  
Multiple Conditions

Toxin–antitoxin (TA) systems are genetic modules found commonly in bacterial genomes. HipA is a toxin protein encoded from the hipBA TA system in the genome of Escherichia coli. Ectopic expression of hipA induces cell growth arrest. Unlike the cell growth arrest caused by other TA toxins, cells resume growth from the HipA-induced cell growth arrest phase after a defined period of time. In this article, we describe the change in the length of growth arrest while cells undergo repeated cycles of hipA induction, growth arrest and regrowth phases. In the multiple conditions tested, we observed that the length of growth arrest became successively shorter for each round of induction. We verified that this was not due to the appearance of HipA-resistant mutants. Additionally, we identified conditions, such as the growth phase of the starting culture and growth vessels, that alter the length of growth arrest. Our results showed that the length of HipA-induced growth arrest was dependent on environmental factors—in particular, the past growth environment of cells, such as a previous hipA induction. These effects lasted even after multiple rounds of cell divisions, indicating the presence of cellular “memory” that impacts cells’ response to HipA-induced toxicity.

scholarly journals Modulation of Cell Proliferation by Cytokeratins K10 and K16

1999 ◽  
Vol 19 (4) ◽  
pp. 3086-3094 ◽  
Author(s):  
Jesús M. Paramio ◽  
M. Llanos Casanova ◽  
Carmen Segrelles ◽  
Sybille Mittnacht ◽  
E. Birgitte Lane ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Ectopic Expression ◽  
Growth Arrest ◽  
Human Keratinocytes ◽  
Cytoskeletal Proteins ◽  
Viral Oncoproteins ◽  
Cell Growth Arrest ◽  
Transfected Cells ◽  
Inhibitory Function

ABSTRACT The members of the large keratin family of cytoskeletal proteins are expressed in a carefully regulated tissue- and differentiation-specific manner. Although these proteins are thought to be involved in imparting mechanical integrity to epithelial cells, the functional significance of their complex differential expression is still unclear. Here we provide new data suggesting that the expression of particular keratins may influence cell proliferation. Specifically, we demonstrate that the ectopic expression of K10 inhibits the proliferation of human keratinocytes in culture, while K16 expression appears to promote the proliferation of these cells. Other keratins, such as K13 or K14, do not significantly alter this parameter. K10-induced inhibition is reversed by the coexpression of K16 but not that of K14. These results are coherent with the observed expression pattern of these proteins in the epidermis: basal, proliferative keratinocytes express K14; when they terminally differentiate, keratinocytes switch off K14 and start K10 expression, whereas in response to hyperproliferative stimuli, K16 replaces K10. The characteristics of this process indicate that K10 and K16 act on the retinoblastoma (Rb) pathway, as (i) K10-induced inhibition is hampered by cotransfection with viral oncoproteins which interfere with pRb but not with p53; (ii) K10-mediated cell growth arrest is rescued by the coexpression of specific cyclins, cyclin-dependent kinases (CDKs), or cyclin-CDK complexes; (iii) K10-induced inhibition does not take place in Rb-deficient cells but is restored in these cells by cotransfection with pRb or p107 but not p130; (iv) K16 efficiently rescues the cell growth arrest induced by pRb in HaCaT cells but not that induced by p107 or p130; and (v) pRb phosphorylation and cyclin D1 expression are reduced in K10-transfected cells and increased in K16-transfected cells. Finally, using K10 deletion mutants, we map this inhibitory function to the nonhelical terminal domains of K10, hypervariable regions in which keratin-specific functions are thought to reside, and demonstrate that the presence of one of these domains is sufficient to promote cell growth arrest.

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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