Related Experiment Video

Updated: Dec 27, 2025

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

11.4K

Troglitazone, a Selective Ligand for PPARγ, Induces Cell-cycle Arrest in Human Oral SCC Cells

Masahiro Saito1, Yuki Fujita1, Nobuyuki Kuribayashi1,2

  • 1Department of Oral and Maxillofacial Surgery, Dokkyo Medical University School of Medicine, Tochigi, Japan.

Anticancer Research
|March 6, 2020
PubMed
Abstract

Insights

Troglitazone (TRO) inhibits oral squamous cell carcinoma (SCC) growth by arresting the cell cycle at G1 phase, without inducing apoptosis. This clarifies the role of Peroxisome proliferator-activated receptor γ (PPARγ) in oral SCC progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Oral squamous cell carcinoma (OSCC) is a significant global health concern.
  • The role of Peroxisome proliferator-activated receptor γ (PPARγ) in OSCC remains incompletely understood.
  • Troglitazone (TRO), a PPARγ ligand, has shown potential anti-cancer effects.

Purpose of the Study:

  • To elucidate the role of PPARγ and its ligand, troglitazone (TRO), in oral squamous cell carcinoma (OSCC).
  • To investigate the impact of TRO on OSCC cell growth and cell-cycle progression.

Main Methods:

  • Examined PPARγ gene expression in 47 human oral SCC tissues and two OSCC cell lines (CA9-22, HSC-4).
  • Assessed the effects of TRO on OSCC cell proliferation and cell-cycle distribution.
  • Utilized quantitative real-time PCR for mRNA detection.

Main Results:

  • PPARγ mRNA was detected in 20 of 47 oral SCC tissues and both cell lines.
  • TRO significantly suppressed oral SCC cell growth.
  • TRO treatment led to G1 phase cell-cycle arrest in CA9-22 cells, with decreased S and G2-M phase fractions, but did not induce apoptosis.

Conclusions:

  • Troglitazone inhibits oral SCC cell growth by arresting the cell cycle at the G1 phase.
  • TRO does not induce apoptosis in oral SCC cells.
  • These findings highlight PPARγ signaling as a potential therapeutic target in oral cancer.
Keywords:
G1 arrestPeroxisome proliferator-activated receptor γapoptosisoral SCCtroglitazone

More Related Videos

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells07:22

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells

Published on: March 28, 2013

39.4K
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

14.0K

Related Concept Videos

Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
533
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
759
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...
5.5K
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are...
468
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
489
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
510