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- Title
Oxobedfordia acid reduces colon cancer cell viability through apoptosis induction and inhibits colon cancer growth in mice model.
- Authors
Songbo Ma; Zhi Yu; Mingliang Zhang; Jianwen Ma
- Abstract
Purpose: Colon cancer is amongst the most commonly diagnosed carcinoma globally and ranks 3rd highest of all the kinds of tumors. In the present study effect of oxobedfordia acid on colon cancer cell viability and colorectal tumor growth in vivo was investigated. Methods: Cytotoxicity of oxobedfordia acid in SW480, HCT116, and FHC cells was evaluated by MTT assay. Colon cancer in the mice was induced by implanting subcutaneously 2 x 106 HT-29 cells/mouse in the right flank. Various parameters, including cell viability, tumor growth and expression levels of cancer factors, were also assessed. Results: Treatment with oxobedfordia acid significantly reduced viability in SW480 and HCT116 cells (p < 0.05). Furthermore, oxobedfordia acid caused increased miR-331-3p levels in cells. Moreover, oxobedfordia acid caused a significant reduction in NRP2 expression and increased apoptosis induction in SW480 and HCT116 cells. Oxobedfordia acid treatment for 48 h significantly increased p53 and p-c-Jun levels, but reduced Bcl-2 expression in cells (p < 0.05). In the mouse model of colon cancer, oxobedfordia acid significantly retarded tumor growth. Furthermore, in oxobedfordia acid-treated mice, expression of miR-331-3p was elevated while NRP2 level was lowered when compared with control group (p < 0.05). Conclusion: Oxobedfordia acid treatment suppresses colon cancer cell viability and inhibits tumor growth in mice through enhancement of miR-331-3p and reduction in NRP2 expression. Hence, oxobedfordia acid can potentially be developed as an agent for the management of colorectal cancer.
- Subjects
COLON cancer; TUMOR growth; CELL survival; ANIMAL disease models; LABORATORY mice
- Publication
Tropical Journal of Pharmaceutical Research, 2022, Vol 21, Issue 6, p1215
- ISSN
1596-5996
- Publication type
Article
- DOI
10.4314/tjpr.v21i6.12