Abstract |
Lung cancer is the foremost cause of cancer mortality and a growing economic burden worldwide. Rhizoma paridis saponins (RPS) have been reported to exhibit potential anti- tumor effects on many kinds of tumor models. The present study was designed to investigate the mechanism-based chemopreventive nature of RPS against DEN-induced lung carcinogenesis in Kunming mice. As a result, the treatment with RPS reduced the severity of pulmonary histopathology. The mechanism of its antitumor effect involved in (a) reducing oxidative stress injury through up-regulating activities of CAT and SOD; (b) down-regulating the levels of inflammatory factors, like TNF-α, IL6, COX-2, and PGE2; (c) activation of caspase-3 and up-regulating the pro-apoptotic protein Bax; (d) decreasing the expression of PCNA; (e) depressing the expression of cancer stem cells marker CD133; (f) suppressing aberrant expression of cytokeratin 8 and 18; and (g) inhibiting EGFR/ PI3 K/Akt, EGFR/Ras/Erk and NF-κB pathways. Taken together, RPS would be a potent agent inhibiting lung tumor in the future.
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Authors | Shuli Man, Jing Li, Peiyu Qiu, Jing Liu, Zhen Liu, Long Ma, Wenyuan Gao |
Journal | Molecular carcinogenesis
(Mol Carcinog)
Vol. 56
Issue 5
Pg. 1405-1413
(05 2017)
ISSN: 1098-2744 [Electronic] United States |
PMID | 27991692
(Publication Type: Journal Article)
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Copyright | © 2017 Wiley Periodicals, Inc. |
Chemical References |
- Antineoplastic Agents, Phytogenic
- Saponins
- Diethylnitrosamine
- EGFR protein, mouse
- ErbB Receptors
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Topics |
- Animals
- Antineoplastic Agents, Phytogenic
(pharmacology)
- Apoptosis
(drug effects)
- Cell Proliferation
(drug effects)
- Diethylnitrosamine
(toxicity)
- ErbB Receptors
(metabolism)
- Liliales
(chemistry)
- Lung Neoplasms
(chemically induced, drug therapy, pathology)
- Male
- Mice
- Neoplasms, Experimental
(drug therapy)
- Neoplastic Stem Cells
(drug effects, pathology)
- Oxidative Stress
(drug effects)
- Rhizome
(chemistry)
- Saponins
(pharmacology)
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