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Updated: Mar 21, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
AS160 controls eukaryotic cell cycle and proliferation by regulating the CDK inhibitor p21
Pianchou Gongpan1,2, Yanting Lu1,2, Fang Wang1,2
1a State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany , Chinese Academy of Sciences , Kunming , Yunnan , P.R. China.
Abstract:
AS160 (TBC1D4) has been implicated in multiple biological processes. However, the role and the mechanism of action of AS160 in the regulation of cell proliferation remain unclear. In this study, we demonstrated that AS160 knockdown led to blunted cell proliferation in multiple cell types, including fibroblasts and cancer cells. The results of cell cycle analysis showed that these cells were arrested in the G1 phase. Intriguingly, this inhibition of cell proliferation and the cell cycle arrest caused by AS160 depletion were glucose independent. Moreover, AS160 silencing led to a marked upregulation of the expression of the cyclin-dependent kinase inhibitor p21. Furthermore, whereas AS160 overexpression resulted in p21 downregulation and rescued the arrested cell cycle in AS160-depeleted cells, p21 silencing rescued the inhibited cell cycle and proliferation in the cells. Thus, our results demonstrated that AS160 regulates glucose-independent eukaryotic cell proliferation through p21-dependent control of the cell cycle, and thereby revealed a molecular mechanism of AS160 modulation of cell cycle and proliferation that is of general physiological significance.
Insights
AS160 (TBC1D4) regulates cell proliferation independently of glucose by controlling the cell cycle via p21. This study reveals a key mechanism for AS160 in cell cycle and proliferation.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- AS160 (TBC1D4) is involved in various biological processes.
- Its precise role in regulating cell proliferation and its mechanism of action are not fully understood.
Purpose of the Study:
- To elucidate the role and mechanism of AS160 in regulating eukaryotic cell proliferation.
- To investigate the relationship between AS160, cell cycle, and the cyclin-dependent kinase inhibitor p21.
Main Methods:
- AS160 knockdown and overexpression in fibroblasts and cancer cells.
- Cell cycle analysis using flow cytometry.
- Western blotting to assess p21 and AS160 expression levels.
- p21 silencing experiments.
Main Results:
- AS160 depletion inhibited cell proliferation and caused G1 phase cell cycle arrest in a glucose-independent manner.
- AS160 silencing led to increased p21 expression.
- AS160 overexpression decreased p21 levels and rescued cell cycle arrest.
- p21 silencing rescued proliferation and cell cycle progression in AS160-depleted cells.
Conclusions:
- AS160 regulates glucose-independent cell proliferation through p21-dependent cell cycle control.
- This study reveals a novel molecular mechanism for AS160 in modulating cell cycle and proliferation with broad physiological relevance.
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