Related Experiment Video
Updated: Sep 26, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
Published on: May 14, 2016
Pogostemon Cablin Aqueous Extract (PCAE) Induces Mitotic Delay by Downregulating CDC2/Cyclin B1 in TNBC Cells
Kun-Ming Rau1, Kuan-Ting Lee2, Yung-Shun Su2,3,4,5
1Department of Hematology Oncology, E-Da Cancer Hospital, I-Shou University, Kaohsiung 824, Taiwan, isu.edu.tw.
Abstract:
Pogostemon cablin (PC) is a traditional medicinal herb with diverse pharmacological activities, including reported anticancer effects. However, its therapeutic potential in triple-negative breast cancer (TNBC) many unknowns remain. In this article, we investigated the antiproliferative activity of PC aqueous extract (PCAE) in MDA-MB-231 TNBC cells and explored the factors responsible for its anticancer effects. The cytotoxicity was evaluated by the MTT method, whereas apoptosis, cell-cycle distribution, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and mitotic progression were analyzed. The expression of G 2/M regulatory proteins was examined by western blotting. PCAE significantly suppressed the growth of TNBC cells in a dosage- and time-dependent manner without inducing significant apoptosis, mitochondrial membrane depolarization, or caspase-3 activation. Instead, PCAE markedly increased G 2/M phase accumulation and mitotic index, accompanied by modulation of CDC25C phosphorylation and downregulation of CDC2 and cyclin B1 expression. These molecular alterations indicate that PCAE disrupts mitotic progression through inhibition of the CDC25C-CDC2/cyclin B1 regulatory axis. Collectively, our findings demonstrate that PCAE inhibits TNBC cell growth primarily by inducing mitotic delay rather than apoptosis, providing new mechanistic insight into the antitumor activity of PC and a promising therapeutic candidate for TNBC.
Related Concept Videos
Anaphase Promoting Complex
Abnormal Proliferation
Inhibition of Cdk Activity
Drugs that Stabilize Microtubules
Mitogens and the Cell Cycle
Positive Regulator Molecules
