Related Experiment Video
Updated: Dec 8, 2025
Evaluation of Stem Cell Properties in Human Ovarian Carcinoma Cells Using Multi and Single Cell-based Spheres Assays
Published on: January 3, 2015
6,12-Diphenyl-3, 9-diazatetraasterane-1, 5, 7, 11-tetracarboxylate Inhibits Proliferation, Migration and Promotes
Pingping Chen1, Huibing Wang1, Meng Li1
1Department of Pharmacology, College of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang, 050200 Hebei Province, China.
Abstract:
6,12-Diphenyl-3,9-diazatetraasterane-1, 5, 7, 11-tetracarboxylate (DDTC) has been synthesized by the photodimerization of 4-phenyl-1,4-dihydropyridine-3,5-dicarboxylate. The potential of theercvantitumor activity and mechanism were investigated in vitro using MTT assay in human lung cancer cell line A549, ovarian cancer cell lines SKOV3 and A2780, breast cancer cell line MCF-7, gastric cancer cell line BGC-823, colon cancer cell line HT29, prostate cancer cell line DU145, and liver cancer cell line SMMC7721. The results show that DDTC can inhibit the growth of ovarian cancer SKOV3 and A2780 cells. The best IC50 value is approximately 5.29 ± 0.38 and 4.29 ± 0.39 μM, respectively. DDTC induced the cell cycle arrest in the G2 phase by flow cytometric analysis. The migration and invasion of ovarian cancer SKOV3 and A2780 cells were inhibited by DDTC. DDTC could increase the expression protein level of E-cadherin in A2780 cells and ascend the expression protein and mRNA levels of E-cadherin in SKOV3 cells. DDTC could also decrease the protein and mRNA expression of EMT (epithelial-to-mesenchymal transition) markers of N-cadherin and Vimentin. mRNA and protein expression level of checkpoint kinase 1 (Chk1) were significantly increased and expressions of cyclin-dependent kinase (CDK1) and cell division cycle 25a (Cdc25a) were decreased in the SKOV3 and A2780 cell lines. Moreover, DDTC induced apoptosis by the cleavage and activation of caspase 3 and caspase 9.
Insights
6,12-Diphenyl-3,9-diazatetraasterane-1, 5, 7, 11-tetracarboxylate (DDTC) shows significant antitumor activity against ovarian cancer cells. This compound inhibits cell growth, migration, and invasion, while inducing apoptosis and cell cycle arrest.
Area of Science:
- Medicinal Chemistry
- Cancer Biology
- Molecular Pharmacology
Background:
- The synthesis of novel compounds with potential anticancer properties is crucial for developing new therapeutic strategies.
- 6,12-Diphenyl-3,9-diazatetraasterane-1, 5, 7, 11-tetracarboxylate (DDTC) is a newly synthesized compound with a unique tetraasterane structure.
Purpose of the Study:
- To investigate the in vitro antitumor activity and underlying mechanisms of DDTC against various human cancer cell lines.
- To evaluate DDTC's efficacy specifically in ovarian cancer models.
Main Methods:
- Synthesis of DDTC via photodimerization.
- In vitro evaluation using MTT assay across multiple cancer cell lines (A549, SKOV3, A2780, MCF-7, BGC-823, HT29, DU145, SMMC7721).
- Flow cytometry for cell cycle analysis, Western blotting and RT-qPCR for protein and gene expression analysis (E-cadherin, N-cadherin, Vimentin, Chk1, CDK1, Cdc25a, Caspase 3, Caspase 9).
Main Results:
- DDTC demonstrated significant inhibitory effects on ovarian cancer cell lines SKOV3 and A2780, with IC50 values of 5.29 ± 0.38 μM and 4.29 ± 0.39 μM, respectively.
- DDTC induced G2 phase cell cycle arrest, inhibited cell migration and invasion, and modulated epithelial-to-mesenchymal transition (EMT) markers by increasing E-cadherin and decreasing N-cadherin and Vimentin.
- DDTC treatment led to increased expression of Chk1 and apoptosis via caspase activation (caspase 3 and 9), while decreasing CDK1 and Cdc25a levels.
Conclusions:
- DDTC exhibits potent in vitro antitumor activity, particularly against ovarian cancer.
- The mechanism involves cell cycle arrest, inhibition of EMT and metastasis, and induction of apoptosis.
- DDTC represents a promising candidate for further investigation as an ovarian cancer therapeutic agent.
