Andrographolide Induces ROS-dependent Apoptosis and Suppresses STAT3 Phosphorylation in Primary Effusion Lymphoma Cells
2
Issued Date
2025-12-01
Resource Type
eISSN
17917530
Scopus ID
2-s2.0-105023334794
Pubmed ID
41318115
Journal Title
Anticancer Research
Volume
45
Issue
12
Start Page
5299
End Page
5311
Rights Holder(s)
SCOPUS
Bibliographic Citation
Anticancer Research Vol.45 No.12 (2025) , 5299-5311
Suggested Citation
Mongkon I., Kariya R., Pearngam P., Settha N., Saisuwan K., Boonnate P., Sittithumcharee G., Vaeteewoottacharn K., Saeeng R., Okada S. Andrographolide Induces ROS-dependent Apoptosis and Suppresses STAT3 Phosphorylation in Primary Effusion Lymphoma Cells. Anticancer Research Vol.45 No.12 (2025) , 5299-5311. 5311. doi:10.21873/anticanres.17869 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/113439
Title
Andrographolide Induces ROS-dependent Apoptosis and Suppresses STAT3 Phosphorylation in Primary Effusion Lymphoma Cells
Corresponding Author(s)
Other Contributor(s)
Abstract
BACKGROUND/AIM: Primary effusion lymphoma (PEL) is a rare and aggressive form of non-Hodgkin lymphoma (NHL) with poor prognosis due to resistance to conventional chemotherapy. Andrographolide (AG), a diterpenoid lactone extracted from Andrographis paniculata, has shown anti-tumor activity in several malignancies, but its effects on PEL are unknown. MATERIALS AND METHODS: PEL cell viability was assessed by MTT assay. Apoptosis was evaluated via Annexin V/PI staining and caspase activation. ROS generation was measured by DCFH-DA staining. Protein expression changes were analyzed by Western blotting. To determine the roles of ROS and caspases, cells were co-treated with a reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) or the pan-caspase inhibitor Q-VD-OPh. AG's in vivo effects were tested in a xenograft mouse model. RESULTS: AG inhibited PEL cell proliferation in a dose- and time-dependent manner. Apoptosis was mediated via ROS production and caspase activation. STAT3 phosphorylation was suppressed in a ROS-dependent manner. In vivo, AG (500 mg/kg/day, oral gavage) significantly reduced tumor burden without observable toxicity. CONCLUSION: AG exerts anti-tumor effects against PEL by inducing ROS-dependent apoptosis and suppressing STAT3 signaling. These findings suggest that AG may serve as a promising therapeutic agent for PEL.