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Updated: Feb 10, 2026
Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
Published on: April 13, 2018
Artesunate promotes G2/M cell cycle arrest in MCF7 breast cancer cells through ATM activation
Lijuan Wen1,2, Lei Liu3, Lina Wen4
1Shenzhen Longgang District Maternal and Child Health Care Hospital, Shenzhen, 518000, Guangdong, People's Republic of China.
Background:
Recent studies have revealed that artesunate (ART) has clear anti-tumor activity, suggesting that it could be a good candidate chemotherapeutic agent. In this study, we researched the inhibitory effect of ART on MCF7 cells and explored the possible mechanisms.
Methods:
MTT assay was used to detect the effect of ART on the proliferation of MCF7 cells. Crystal violet staining was used to observe morphological and quantitative changes. Flow cytometry was used to detect the cell cycle of the drug-acting MCF7 cells. In addition, western blotting was used to detect the drug influence on expression of the ATM, phospho-ATM(S1981), H2AX, γH2AX(S139), CHK2 and phospho-CHK2(T68), cdc25C, and phospho-cdc25C(S216).
Results:
In the experimental groups, the proliferation of MCF7 cells was inhibited in a dose-dependent manner and the original cell morphology was lost. The number of G2/M phase cells in the experimental groups increased significantly, and the expression of DNA damage response-associated proteins was significantly increased, such as phospho-ATM(S1981), γH2AX(S139), phospho-CHK2(T68), and phospho-cdc25C(S216).
Conclusions:
ART can inhibit cell proliferation and promote G2/M arrest in MCF7 cells through ATM activation and the ensuing "ATM-Chk2-Cdc25C" pathway, thus implicating ART as a novel candidate for breast cancer chemotherapy.
Insights
Artesunate (ART) inhibits breast cancer MCF7 cell proliferation and induces G2/M arrest. This occurs via the ATM-Chk2-Cdc25C pathway, suggesting ART as a potential chemotherapy agent.
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Artesunate (ART) exhibits anti-tumor properties, positioning it as a potential chemotherapeutic agent.
- This study investigates the inhibitory effects and underlying mechanisms of ART on MCF7 breast cancer cells.
Purpose of the Study:
- To evaluate the impact of ART on MCF7 cell proliferation and morphology.
- To elucidate the cell cycle effects of ART in MCF7 cells.
- To determine ART's influence on DNA damage response pathways.
Main Methods:
- MTT assay for proliferation assessment.
- Crystal violet staining for morphological and quantitative analysis.
- Flow cytometry for cell cycle analysis.
- Western blotting to examine key protein expression (ATM, Chk2, cdc25C, and DNA damage markers).
Main Results:
- ART dose-dependently inhibited MCF7 cell proliferation and altered cell morphology.
- Significant G2/M phase arrest was observed in ART-treated cells.
- Increased expression of DNA damage response proteins (phospho-ATM, γH2AX, phospho-Chk2, phospho-cdc25C) was detected.
Conclusions:
- ART effectively inhibits MCF7 cell proliferation and induces G2/M arrest.
- The mechanism involves ATM activation and the "ATM-Chk2-Cdc25C" signaling pathway.
- ART shows promise as a novel therapeutic candidate for breast cancer treatment.
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