Related Experiment Video
Updated: Dec 3, 2025
Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
Published on: May 14, 2016
CCL113, a novel sulfonamide, induces selective mitotic arrest and apoptosis in HeLa and HepG2 cells
Ruirong Yi1, Yoshifumi Ohno1, Zheng Tian1
1Department of Molecular Virology, Graduate School of Medicine, Chiba University, Chuo‑ku, Chiba 260‑8670, Japan.
Abstract:
Targeting cell‑cycle regulation to hinder cancer cell proliferation is a promising anticancer strategy. The present study investigated the effects of a novel sulfonamide, CCL113, on cell cycle progression in cancer cell lines (HeLa and HepG2), a noncancerous cell line (Vero) and a normal human fibroblast cell line (TIG‑1‑20). The present results showed that treatment with CCL113 significantly decreased the viability of the cancer cells. FACS analyses showed that CCL113 treatment increased the proportion of cancerous and noncancerous cells in the G2/M phase. Analyses of cell cycle regulatory proteins showed that CCL113 treatment inhibited the activity of CDK1 in HeLa cells, possibly due to the decrease in the level of Cdc25B/C proteins and arrest in the M phase. Using time‑lapse imaging‑assisted analyses of HeLa and Vero cells expressing fluorescent ubiquitination‑based cell cycle indicator (FUCCI), it was observed that CCL113 treatment led to a prolonged G2 phase at the G2/M checkpoint and arrest in the M phase in both cell lines. This possibly activated the DNA damage response in noncancerous cells, while inducing mitotic arrest leading to apoptosis in the cancer cells. The results of molecular docking studies suggested that CCL113 might have the potential to bind to the taxol‑binding site on β‑tubulin. In conclusion, CCL113 holds potential as a reliable anticancer drug due to its ability to induce mitotic arrest followed by apoptosis of cancer cells and to activate the DNA damage response in noncancerous cells, thereby facilitating exit from the cell cycle.
Insights
The novel sulfonamide CCL113 effectively reduces cancer cell viability by halting cell division at the G2/M phase. This compound induces mitotic arrest and apoptosis in cancer cells while activating DNA damage response in normal cells.
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Targeting cell-cycle regulation is a key anticancer strategy.
- Novel sulfonamides represent a potential class of anticancer agents.
- Understanding drug effects on cell cycle progression is crucial.
Purpose of the Study:
- To investigate the effects of the novel sulfonamide CCL113 on cell cycle progression.
- To evaluate CCL113's impact on cancer and noncancerous cell lines.
- To elucidate the mechanism of action of CCL113 in cancer therapy.
Main Methods:
- Cell viability assays on HeLa, HepG2, Vero, and TIG-1-20 cells.
- Flow cytometry (FACS) analysis for cell cycle phase distribution.
- Western blot analysis of cell cycle regulatory proteins (e.g., CDK1, Cdc25B/C).
- Time-lapse imaging with Fluorescent Ubiquitination-Based Cell Cycle Indicator (FUCCI).
- Molecular docking studies targeting beta-tubulin.
Main Results:
- CCL113 significantly decreased viability in cancer cell lines (HeLa, HepG2).
- CCL113 induced G2/M phase arrest in both cancer and noncancerous cells.
- Inhibition of CDK1 activity and reduction of Cdc25B/C levels observed in HeLa cells.
- Prolonged G2 phase and M phase arrest confirmed by FUCCI imaging.
- Molecular docking suggests potential binding to the taxol-binding site on beta-tubulin.
Conclusions:
- CCL113 demonstrates potential as an anticancer drug by inducing mitotic arrest and apoptosis in cancer cells.
- CCL113 activates DNA damage response in noncancerous cells, promoting cell cycle exit.
- The drug's mechanism involves disruption of cell cycle regulation at the G2/M checkpoint.
- Potential interaction with beta-tubulin suggests a possible anti-mitotic mechanism.
More Related Videos
13:20Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
Published on: July 17, 2018
11:49Author Spotlight: Establishing CENP-E Knockout HeLa Cells – A Novel Approach to Study Kinesin-7 CENP-E Biology and its Inhibitors
Published on: June 23, 2023
