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Author Spotlight: Developing Acetyl-Click Assay for HAT1 Inhibitor Screening
Published on: January 26, 2024
Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle
Xiao Han1, Ling Liu1, Jing Li1
1Department of Medical Genetic and Prenatal Diagnosis, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Abstract:
Ovarian cancer (OC) is the most common cause of gynecological cancer-related death. Histone acetyltransferase 1 (HAT1) has generated interest as a potential target for therapy due to it being involved in a variety of diseases, including cancer. However, to the best of our knowledge, the role of HAT1 in OC has not yet been investigated. In the present study, HAT1 was upregulated in OC and the high expression of HAT1 was associated with unfavorable prognosis. The transcription factor forkhead box protein A1 (FOXA1) transcriptionally regulated HAT1 expression. Furthermore, HAT1 knockdown in OC cells significantly suppressed cell proliferation and colony formation. In addition, the inhibition of HAT1 promoted cell cycle arrest, and reduced cyclin-dependent kinase (CDK)2, CDK4 and cyclin E levels in OC cells. Taken together, the present data suggested that HAT1 served an oncogenic role in OC; therefore, HAT1 may represents a new potential therapeutic target in OC treatment.
Insights
Histone acetyltransferase 1 (HAT1) is upregulated in ovarian cancer (OC), promoting cell growth. Inhibiting HAT1 suppressed OC cell proliferation and may offer a new therapeutic target for ovarian cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Ovarian cancer (OC) is a leading cause of gynecological cancer mortality.
- Histone acetyltransferase 1 (HAT1) is implicated in various diseases, including cancer, but its role in OC is unexplored.
Purpose of the Study:
- To investigate the role of HAT1 in ovarian cancer.
- To determine the prognostic significance of HAT1 expression in OC.
- To explore the regulatory mechanisms and functional impact of HAT1 in OC cells.
Main Methods:
- Analysis of HAT1 expression in OC tissues.
- Correlation of HAT1 expression with patient prognosis.
- Investigation of the transcriptional regulation of HAT1 by forkhead box protein A1 (FOXA1).
- Assessment of HAT1 knockdown effects on OC cell proliferation, colony formation, and cell cycle progression.
- Measurement of cell cycle-related proteins, including cyclin-dependent kinase (CDK)2, CDK4, and cyclin E.
Main Results:
- HAT1 was found to be upregulated in OC.
- High HAT1 expression correlated with unfavorable prognosis in OC patients.
- FOXA1 was identified as a transcriptional regulator of HAT1.
- HAT1 knockdown significantly inhibited OC cell proliferation and colony formation.
- HAT1 inhibition induced cell cycle arrest and decreased levels of CDK2, CDK4, and cyclin E.
Conclusions:
- HAT1 plays an oncogenic role in ovarian cancer.
- HAT1 expression is regulated by FOXA1.
- HAT1 represents a potential novel therapeutic target for ovarian cancer treatment.
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