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Updated: Jun 14, 2026

Assays for Validating Histone Acetyltransferase Inhibitors
Published on: August 6, 2020
Effects of tyroservatide on histone acetylation in lung carcinoma cells
Qiong Xu1, Rong Lu, Zhi-Feng Zhu
1Department of Immunology, Tianjin Medical University, Tianjin, China.
Abstract:
Tyroservatide (YSV) is an active, low-molecular weight polypeptide shown to have antitumor effects on experimental hepatocarcinoma and lung carcinoma. The focus of our study was to observe the effects of YSV on several human lung carcinoma cell lines and explore its antitumor mechanism via its effect on histone acetylation. Our results showed that YSV significantly inhibited the proliferation of human lung carcinoma A549, NCIH460, NCIH292 and NCIH1299 cells, induced G(0) /G(1) cell cycle arrest and increased protein and mRNA levels of p21 and p27. Moreover, YSV treatment significantly inhibited histone deacetylase (HDAC) activity and resulted in the accumulation of acetylated histones H3 and H4 in total cellular chromatin and p21 gene-associated chromatin regions. Together these data suggest that the antitumor effects of YSV might be mediated by its inhibition of HDAC activity, selectively upregulating the expression of p21 by increasing the acetylation of histones associated with p21 gene regions, resulting in an induction of G₀/G₁ cell cycle arrest and inhibition of the proliferation of tumor cells. Our findings demonstrate that YSV may exhibit potent therapeutical effects on lung carcinoma.
Insights
Tyroservatide (YSV) effectively combats lung carcinoma by inhibiting histone deacetylase (HDAC) activity. This mechanism halts tumor cell proliferation and induces cell cycle arrest, suggesting YSV
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Tyroservatide (YSV) is a low-molecular weight polypeptide with demonstrated antitumor effects.
- Previous studies indicated YSV's efficacy against experimental hepatocarcinoma and lung carcinoma.
Purpose of the Study:
- To investigate the effects of Tyroservatide (YSV) on human lung carcinoma cell lines.
- To elucidate the antitumor mechanism of YSV, focusing on its impact on histone acetylation.
Main Methods:
- Exposure of human lung carcinoma cell lines (A549, NCIH460, NCIH292, NCIH1299) to YSV.
- Assessment of cell proliferation, cell cycle distribution, and protein/mRNA levels of p21 and p27.
- Measurement of histone deacetylase (HDAC) activity and histone acetylation levels (H3, H4) in total and gene-specific chromatin.
Main Results:
- YSV significantly inhibited the proliferation of all tested human lung carcinoma cell lines.
- YSV induced G(0)/G(1) cell cycle arrest and increased p21 and p27 expression.
- YSV inhibited HDAC activity, leading to increased histone H3 and H4 acetylation, particularly in p21 gene regions.
Conclusions:
- YSV exhibits potent antitumor effects on human lung carcinoma.
- The mechanism involves HDAC inhibition, leading to enhanced histone acetylation, p21 upregulation, and cell cycle arrest.
- YSV demonstrates potential as a therapeutic agent for lung carcinoma.
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