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Published on: August 6, 2020
Damnacanthus giganteus extract block diffuse large b-cell lymphoma proliferation and EMT by regulating mitochondrial
Peng Yang1, GuangYun Zhou2, XiuMei Ma3
1Science and Technology Dept, Guangxi International Zhuang Medicine Hospital Affiliated to Guangxi University of Chinese Medicine, Guangxi Zhuang Autonomous Region, No. 8 Qiuyue Road, Wuxiang New District,, Nanning City, 530201, China.
Background:
In non-Hodgkin's lymphoma, diffuse large b-cell lymphoma (DLBCL) is one of the most prevalent and commonly diagnosed subtypes. There is a need to develop more effective drugs since the currently approved drugs still have limitations.
Methods:
DLBCL cell lines were intervened with different concentrations of Damnacanthus giganteus extract (DGE). The malignant phenotype of DLBCL cells was detected by CCK-8, colony formation assay, AnnexinV-PI double staining assay, and Transwell. The effect of DGE on the in vivo growth of DLBCL cells was assessed by nude mice transplantation tumor assay and immunohistochemistry. Cellular mitochondrial function was assessed by measuring mitochondrial ROS levels, MMP, and ATP production, and glycolysis was assessed by determining glucose uptake and lactate production. The changes of epithelial-mesenchymal transition (EMT) markers were evaluated via Western blot.
Results:
Intervention with low-toxicity concentrations of DGE significantly inhibited proliferative capacity and clonogenic potential in DLBCL cells while concurrently enhancing apoptosis and cisplatin sensitivity. DGE treatment also suppressed migratory and invasive behaviors, accompanied by downregulation of mesenchymal markers N-cadherin and Vimentin. In vivo studies confirmed therapeutic efficacy, with DGE monotherapy showing marked tumor growth suppression and synergistic activity with cisplatin. Mechanistically, DGE exacerbated mitochondrial dysfunction and suppressed glycolysis. This mitochondrial impairment phenotype elicited by DGE treatment was recapitulated using the mitochondrial complex I inhibitor Rotenone, which similarly induced proliferation inhibition and EMT modulation. Furthermore, the ROS scavenger N-acetylcysteine partially rescued DGE-induced cellular alterations, including proliferation and EMT suppression.
Conclusion:
Our study demonstrates for the first time that DGE effectively suppresses tumor proliferation and EMT during DLBCL progression. These antitumor effects appear to be mediated through modulation of mitochondrial function and glycolysis. These findings position DGE as a promising novel therapeutic candidate for DLBCL treatment, meriting immediate clinical translation and further evaluation.
Insights
Damnacanthus giganteus extract (DGE) effectively suppresses diffuse large b-cell lymphoma (DLBCL) tumor growth and metastasis. DGE targets mitochondrial function and glycolysis, showing promise as a novel therapeutic for DLBCL.
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Diffuse large b-cell lymphoma (DLBCL) is a prevalent non-Hodgkin's lymphoma subtype.
- Current treatments for DLBCL have limitations, necessitating novel therapeutic strategies.
- There is a need for more effective drugs to combat DLBCL progression.
Purpose of the Study:
- To investigate the anti-cancer effects of Damnacanthus giganteus extract (DGE) on DLBCL.
- To elucidate the mechanisms underlying DGE's therapeutic potential in DLBCL.
- To evaluate DGE as a potential novel therapeutic candidate for DLBCL treatment.
Main Methods:
- DLBCL cell lines were treated with varying concentrations of DGE.
- Cell proliferation, apoptosis, migration, and invasion were assessed using CCK-8, colony formation, AnnexinV-PI, and Transwell assays.
- In vivo tumor growth was evaluated in nude mice, and molecular mechanisms involving mitochondrial function, glycolysis, and epithelial-mesenchymal transition (EMT) were analyzed.
Main Results:
- DGE significantly inhibited DLBCL cell proliferation and clonogenic potential at low, non-toxic concentrations.
- DGE treatment enhanced apoptosis and cisplatin sensitivity, while suppressing migration and invasion.
- In vivo studies demonstrated DGE's efficacy in suppressing tumor growth, both as monotherapy and in combination with cisplatin, by impairing mitochondrial function and glycolysis.
Conclusions:
- DGE demonstrates significant antitumor activity against DLBCL by suppressing proliferation and EMT.
- The observed effects are mediated through the modulation of mitochondrial function and glycolysis.
- DGE represents a promising novel therapeutic agent for DLBCL, warranting further clinical investigation.
