Related Experiment Video
Updated: May 3, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
[Rosiglitazone inhibits human HepG2 cell proliferation via PI3K/PTEN/Akt signaling pathway]
Meng Zhang1, Li Peng, Zhibin Qiao
1Department of Hepatobiliary Surgery, Fourth Affiliated Hospital, Hebei Medical University, Shijiazhuang 050011, China.
Objective:
To investigate the effects of rosiglitazone (ROZ) on proliferation and cell cycle of human hepatocellular carcinoma cell line HepG2 and explore the underlying mechanisms by detecting the related proteins.
Methods:
After treated with ROZ of different concentrations, HepG2 cells were tested for the changes in the cell proliferation by MTT assay and in the cell cycle by flow cytometry. Western blotting and RT-PCR were performed to measure the expressions of PTEN, pAkt, S phase kinase associated protein 2 (Skp2) and P27(kip1); at protein and mRNA levels, respectively. RESULTS ROZ significantly inhibited HepG2 cell proliferation in a concentration-dependent and time-dependent manner (P<0.05). The proportion of HepG2 cells in G0/G1 phase increased, and that in S phase decreased significantly (P<0.05). ROZ reduced the expressions of pAkt and Skp2, and raised the expressions of PTEN and P27(kip1); in HepG2 cells (P<0.05). RT-PCR revealed that ROZ increased the expressions of PTEN mRNA, decreased the expressions of Skp2 mRNA, and had no effect on P27(kip1); mRNA.
Conclusion:
Our study demonstrated that ROZ could inhibit HepG2 cell proliferation and block G0/G1 phase, the mechanisms may be related to the regulation on the expressions of Skp2 and P27(kip1); through the PI3K/PTEN/Akt signaling pathway.
Insights
Rosiglitazone (ROZ) inhibits hepatocellular carcinoma HepG2 cell proliferation and blocks the cell cycle. These effects are linked to the PI3K/PTEN/Akt pathway, impacting Skp2 and P27(kip1) protein expression.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Hepatocellular carcinoma (HCC) is a significant global health concern.
- Understanding the molecular mechanisms underlying HCC proliferation is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the effects of rosiglitazone (ROZ) on HepG2 cell proliferation and cell cycle.
- To explore the underlying molecular mechanisms involving key proteins and signaling pathways.
Main Methods:
- HepG2 cells were treated with varying concentrations of ROZ.
- Cell proliferation was assessed using MTT assay.
- Cell cycle distribution was analyzed by flow cytometry.
- Protein and mRNA expression levels of PTEN, pAkt, Skp2, and P27(kip1) were measured using Western blotting and RT-PCR.
Main Results:
- ROZ significantly inhibited HepG2 cell proliferation in a dose- and time-dependent manner.
- ROZ treatment led to an increased proportion of cells in the G0/G1 phase and a decrease in the S phase.
- ROZ reduced pAkt and Skp2 expression while increasing PTEN and P27(kip1) expression at the protein level.
- ROZ increased PTEN mRNA and decreased Skp2 mRNA levels, with no significant effect on P27(kip1) mRNA.
Conclusions:
- ROZ effectively inhibits HepG2 cell proliferation and induces G0/G1 cell cycle arrest.
- The observed effects are likely mediated through the PI3K/PTEN/Akt signaling pathway.
- ROZ modulates the expression of Skp2 and P27(kip1), contributing to its anti-cancer effects in HCC.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
Oral Hypoglycemic Agents: Biguanides and Glitazones
Dipeptidyl Peptidase 4 Inhibitors
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Insulin: The Receptor and Signaling Pathways
Glucagon-like Receptor Agonists
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...

