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Telmisartan Exerts Cytotoxicity in Scirrhous Gastric Cancer Cells by Inducing G0/G1 Cell Cycle Arrest
Yoshie Tsujiya1, Motohiro Yamamori1, A I Hasegawa1
1Department of Clinical Pharmacy, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya, Japan.
Background/Aim:
This study aimed to assess the effects of telmisartan (TEL), a potential antitumor agent, and its mechanism of action in the regulation of apoptosis, autophagy, and cell cycle in scirrhous gastric cancer (SGC).
Materials And Methods:
The effect of TEL on the viability and chromatin condensation of OCUM-2M and OCUM-12 cells was assessed. Protein expression and the cell cycle were analysed using western blotting and flow cytometry, respectively.
Results:
TEL inhibited cell proliferation in a dose-dependent manner and increased chromatin condensation and autophagy marker LC3-II levels in OCUM-12 cells. TEL also increased the proportion of cells in the G0/G1 phase transition.
Conclusion:
Apoptosis and autophagy are partially involved in the inhibitory effect of TEL on cell proliferation. Additionally, TEL caused G0/G1 cell cycle arrest. Therefore, TEL could be a promising treatment for SGC.
Insights
Telmisartan (TEL) inhibits scirrhous gastric cancer (SGC) cell proliferation by inducing apoptosis and autophagy. This potential antitumor agent also causes G0/G1 cell cycle arrest, suggesting its promise for SGC treatment.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Scirrhous gastric cancer (SGC) presents unique challenges in treatment.
- Telmisartan (TEL), an angiotensin receptor blocker, has shown potential as an antitumor agent.
- Understanding TEL's mechanism in SGC is crucial for therapeutic development.
Purpose of the Study:
- To evaluate the effects of telmisartan (TEL) on scirrhous gastric cancer (SGC) cells.
- To investigate TEL's mechanism of action, focusing on apoptosis, autophagy, and cell cycle regulation.
- To assess TEL's potential as a therapeutic agent for SGC.
Main Methods:
- Cell viability and chromatin condensation were assessed in SGC cell lines (OCUM-2M, OCUM-12).
- Western blotting was used to analyze protein expression.
- Flow cytometry was employed to determine cell cycle distribution and apoptosis.
Main Results:
- Telmisartan (TEL) inhibited SGC cell proliferation in a dose-dependent manner.
- TEL treatment increased chromatin condensation and the autophagy marker LC3-II in OCUM-12 cells.
- TEL induced a significant increase in cells within the G0/G1 phase, indicating cell cycle arrest.
Conclusions:
- Telmisartan (TEL) exhibits antitumor effects in scirrhous gastric cancer (SGC) through partial induction of apoptosis and autophagy.
- TEL effectively causes G0/G1 cell cycle arrest in SGC cells.
- Telmisartan (TEL) represents a promising therapeutic candidate for scirrhous gastric cancer treatment.
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