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Updated: Jan 15, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
Acrylamide-mediated errors in the cell cycle regulation are associated with altered TORC2 signaling in
Alica Navrátilová1, Marek Kovár2, Lucia Klongová3
1Institute of Nutrition and Genomics , Slovak University of Agriculture , Nitra, Slovakia.
Abstract:
Acrylamide (AA) poses a significant risk to living organisms as it is linked to serious health concerns. AA exposure triggers oxidative stress in cells through elevated ROS and modulation of antioxidant enzymes activities and expression of genes encoding antioxidant enzymes. AA-induced cell proliferation defects are linked to affected cell cycle regulation demonstrated by changes in the expression of genes encoding the major cell cycle regulators cdc2, cdc13, and cdc25, Additionally, cell division defects can be linked to changes in the expression of ark1 and cdc15, and AA-induced errors in chromosome segregation. The stress response involves signaling pathways like MAPKs (Mitogen-activated protein kinases) or the target of rapamycin (TOR) constituting two complexes TORC 1 and 2. As TORC2 manages the cell response to various stresses, its involvement in AA-mediated stress has been demonstrated by changes in the expression of tor1, wat1, ste20, sin1, bit61 encoding TORC2 members, and gad8 encoding a direct Tor1substrate, Gad8. To our surprise, AA has not affected the expression of sty1, which encodes the major stress-regulating kinase of the MAPK pathway in S. pombe. In the presented study we demonstrate, for the first time, that exposure to AA disrupts cellular homeostasis by altering TORC2 signaling and cell cycle regulation ultimately leading to carcinogenesis.
Insights
Acrylamide exposure causes cell damage by disrupting TORC2 signaling and cell cycle regulation. This study reveals acrylamide
Area of Science:
- Cell Biology
- Toxicology
- Molecular Biology
Background:
- Acrylamide (AA) is a toxic compound linked to severe health risks.
- AA exposure induces oxidative stress, affecting cellular functions and gene expression.
- Cell cycle regulation and division are critical processes impacted by AA.
Purpose of the Study:
- To investigate the molecular mechanisms underlying acrylamide-induced cellular damage.
- To explore the role of TORC2 signaling in response to acrylamide exposure.
- To elucidate the link between AA, cellular homeostasis disruption, and carcinogenesis.
Main Methods:
- Gene expression analysis of key regulators involved in cell cycle and stress response pathways.
- Investigated the impact of AA on TORC1 and TORC2 complexes.
- Utilized S. pombe as a model organism to study AA effects.
Main Results:
- AA exposure alters TORC2 signaling pathway components, including tor1, wat1, ste20, sin1, bit61, and gad8.
- AA disrupts cell cycle regulation, affecting genes like cdc2, cdc13, and cdc25.
- AA exposure leads to cell division defects and chromosome segregation errors.
- Unexpectedly, AA did not affect the expression of sty1, a key MAPK pathway kinase in S. pombe.
Conclusions:
- Acrylamide disrupts cellular homeostasis by altering TORC2 signaling and cell cycle regulation.
- These disruptions ultimately contribute to the development of cancer.
- The study provides novel insights into the carcinogenic mechanisms of acrylamide.
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