Maslinic acid induced apoptosis in bladder cancer cells through activating p38 MAPK signaling pathway
Shilong Zhang1, Degang Ding, Xiangsheng Zhang
1Department of Urologic Surgery, People's Hospital of Zhengzhou University, 7 Weiwu Road, Zhengzhou, 450003, China, shilongzhanghn@gmail.com.
Abstract:
Bladder cancer is among the most aggressive human malignant carcinoma and always showed resistance to traditional chemotherapy based on DNA damaging drugs. Unlike the existing drugs that damage nuclear acid molecules, maslinic acid (MA) displays anti-tumor function in various types of cancers by targeting specific intracellular signaling pathways and is regarded as a promising agent for future clinical cancer therapy. However, its effect on bladder cancer is still unknown. In this study, we assessed the influence of MA on survival of bladder cancer cells and the involved mechanisms. MTT assay showed that MA suppressed the viability of bladder cancer cells. We further confirmed the growth-suppressing activity of MA on T24 and 253J xenograft tumor in mouse models. Subsequently, we found that MA induced apoptosis in bladder cancer cells. Based on immunoblotting assay, we determined that p38 MAPK pathway was greatly activated in MA-treated bladder cancer cells. SB203580 inhibition of p38 MAPK rescued the MA-induced apoptosis of bladder cancer cells. In conclusion, we provided evidences that MA efficiently suppressed activation of p38 MAPK pathways and induced apoptosis of bladder cancer cells.
Insights
Maslinic acid (MA) effectively combats bladder cancer by inducing apoptosis, or programmed cell death. This natural compound targets the p38 MAPK pathway, offering a promising new avenue for cancer therapy.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Bladder cancer is an aggressive malignancy often resistant to conventional chemotherapy.
- Maslinic acid (MA) shows anti-tumor potential in various cancers by modulating specific signaling pathways.
- The efficacy of MA in bladder cancer remains unexplored.
Purpose of the Study:
- To investigate the anti-cancer effects of maslinic acid (MA) on bladder cancer cells.
- To elucidate the underlying molecular mechanisms, particularly the involvement of the p38 MAPK pathway.
Main Methods:
- Cell viability was assessed using MTT assays.
- In vivo efficacy was evaluated in T24 and 253J bladder cancer xenograft mouse models.
- Apoptosis induction was analyzed, and p38 MAPK pathway activation was examined via immunoblotting.
Main Results:
- Maslinic acid significantly suppressed bladder cancer cell viability in vitro.
- MA demonstrated growth-suppressing activity in preclinical mouse models.
- MA treatment induced apoptosis in bladder cancer cells, correlating with p38 MAPK pathway activation.
Conclusions:
- Maslinic acid exhibits potent anti-bladder cancer activity by inducing apoptosis.
- The p38 MAPK pathway is a key mediator of MA's anti-tumor effects in bladder cancer.
- MA represents a promising therapeutic candidate for bladder cancer treatment.
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