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.

Anticancer Research
|November 4, 2021
PubMed
Abstract

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.

Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.9K
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
3.8K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.0K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
1.4K