| Title |
Evodiamine activates cellular apoptosis through suppressing PI3K/AKT and activating MAPK in glioma
|
|---|---|
| Published in |
OncoTargets and therapy, March 2018
|
| DOI | 10.2147/ott.s155275 |
| Pubmed ID | |
| Authors |
Rong Wang, Danni Deng, Naiyuan Shao, Yuan Xu, Lian Xue, Ya Peng, Yatian Liu, Feng Zhi |
| Abstract |
Glioblastoma multiforme (GBM) is the most malignant primary tumor of the central nervous system and is associated with a very poor prognosis. No further improvements in outcomes have been reported since radiotherapy-temozolomide therapy was introduced. Therefore, developing new agents to treat GBM is important. This study aimed to evaluate the anti-tumor effect of evodiamine (Evo) on GBM cells, and to determine the underlying mechanisms involved. According to MTT assay results, Evo significantly inhibited the cell proliferation in a time- and dose-dependent manner. Fluorescence microscopy and flow cytometry analyses revealed that Evo induced cell apoptosis in a concentration-dependent manner. Moreover, Evo induced reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP) disruption. Finally, Evo induced apoptosis in cancer cells by suppressing PI3K/AKT signaling and inducing MAPK phosphorylation (p38 and JNK, but not ERK) to regulate apoptotic proteins (Bax, Bcl-2, Cytochrome c, Caspase-3, and PARP). In summary, Evo inhibits cell proliferation by inducing cellular apoptosis via suppressing PI3K/AKT and activating MAPK in GBM; these results indicate that Evo may be regarded as a new approach for GBM treatment. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 19 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 19 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 4 | 21% |
| Student > Bachelor | 3 | 16% |
| Student > Master | 2 | 11% |
| Student > Doctoral Student | 1 | 5% |
| Researcher | 1 | 5% |
| Other | 0 | 0% |
| Unknown | 8 | 42% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 6 | 32% |
| Biochemistry, Genetics and Molecular Biology | 4 | 21% |
| Neuroscience | 1 | 5% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 5% |
| Unknown | 7 | 37% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 15 March 2018.
All research outputs
#22,767,715
of 25,382,440 outputs
Outputs from OncoTargets and therapy
#2,078
of 3,016 outputs
Outputs of similar age
#305,283
of 344,853 outputs
Outputs of similar age from OncoTargets and therapy
#70
of 90 outputs
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