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Hesa-A Effects on Cell Cycle Signaling in Esophageal Carcinoma Cell Line
Nasser Ahmadian1, Roghiyeh Pashaei-Asl2, Nasser Samadi2
1Faculty of Advanced Medical Science Technology, Golestan University of Medical Sciences, Gorgan, Iran.
Abstract:
BACKGROUND Hesa-A is a natural compound with anticancer properties. The exact mechanism of its action in esophageal cancer is not clear, yet. The aim of this study was to evaluate the cell toxicity effect of Hesa-A on the esophageal carcinoma cell lines, KYSE-30, and cell cycle genes expression. METHODS In this study, we tested cell toxicity with MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay and flow cytometry to evaluatet he cell cycle arrest. Real time polymerase chain reaction was used to assess the expression of P53, P16, P21, cyclin D1, and cyclin B1 genes. RESULTS Our results showed that Hesa-A is effective in the expression of cell cycling check point proteins. Hesa-A induced an arrest in G2 phase of esophageal cell cycle. The levels of P53 (>13 times), P21 (>21 times), P16, cyclin B1, and cyclin D1 genes were increased 48 hours after Hesa-A treatment. CONCLUSION P21 and P16 expression were the potential mechanisms for G2 arrest of KYSE-30 esophageal cancer cell line by Hesa-A.
Insights
Hesa-A, a natural compound, effectively inhibits esophageal cancer cell growth by inducing cell cycle arrest at the G2 phase. This anticancer effect is linked to increased expression of key cell cycle regulator genes, P53, P21, and P16.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Hesa-A is a natural compound with demonstrated anticancer properties.
- Its precise mechanism in esophageal cancer remains largely unelucidated.
- Esophageal carcinoma necessitates novel therapeutic strategies.
Purpose of the Study:
- To investigate the cytotoxic effects of Hesa-A on KYSE-30 esophageal cancer cells.
- To analyze the impact of Hesa-A on cell cycle progression and gene expression.
- To identify potential molecular targets of Hesa-A in esophageal cancer.
Main Methods:
- Cytotoxicity was assessed using the MTT assay.
- Cell cycle arrest was evaluated via flow cytometry.
- Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to measure the expression of P53, P16, P21, cyclin D1, and cyclin B1.
Main Results:
- Hesa-A treatment resulted in significant G2 phase cell cycle arrest in KYSE-30 cells.
- The expression of P53, P21, P16, cyclin D1, and cyclin B1 genes was notably upregulated 48 hours post-treatment.
- P53 and P21 levels increased over 13-fold and 21-fold, respectively.
Conclusions:
- Hesa-A exhibits potent anti-esophageal cancer activity.
- The G2 cell cycle arrest induced by Hesa-A is potentially mediated by the upregulation of P21 and P16.
- These findings highlight Hesa-A as a promising candidate for esophageal cancer therapy.
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