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Balkan Journal of Medical Genetics
Volumen 23 (2020): Edición 1 (June 2020)
Acceso abierto
β-Elemene inhibits the proliferation and migration of human glioblastoma cell lines
via
suppressing ring finger protein 135
M Alizada
M Alizada
,
J Li
J Li
,
H Aslami
H Aslami
,
D Yang
D Yang
,
T Korchuganova
T Korchuganova
y
YH Xu
YH Xu
| 26 ago 2020
Balkan Journal of Medical Genetics
Volumen 23 (2020): Edición 1 (June 2020)
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Article Category:
Original Article
Publicado en línea:
26 ago 2020
Páginas:
43 - 49
DOI:
https://doi.org/10.2478/bjmg-2020-0002
Palabras clave
β-Elemene
,
Glioblastoma
,
Migration
,
Proliferation
,
Ring finger protein 135 (RNF135)
,
Tumorigenicity
© 2020 Alizada M, Li J, Aslami H, Yang D, Korchuganova T, Xu YH, published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.
Figure 1
The expression level of RNF135 is suppressed in human glioblastoma cell lines U251, U118, U87 and A172 treated with β-elemene. The data from qRT-PCR (Author: see Abstract) of three independent experimental groups showed that the cell lines treated with β-elemene have a lower level of RNF 135 mRNA than the control group (p <0.05) (A-D). The data from Western blot also confirmed that protein levels of RNF135 were lower in the cell lines that were treated with β-elemene than those of the control group (E-H). Glyceraldehyde 3-phosphate dehydrogenase was used for both qRT-PCR and Western blot as loading control.
Figure 2
Increasing β-elemene treatment dose decreases viability of glioblastoma cells. Human glioblastoma cell lines U251, U118, U87 and A172 were sown at the concentration of 5000 cells per well in 96-well plates and treated with various doses (0, 20, 40, 60, 80 and 100 μg/mL) of β-elemene. The half maximal inhibitory effects (IC50) of the cells were obtained by doses of 47.44, 49.68, 58.41 and 57.36 μg/mL of β-elemene, respectively (A-D). The CCK-8 was utilized to ascertain cell viability and inhibitory effect of β-elemene on the proliferation of the cells. The results are shown as mean ± SD of the three experiments (p <0.05, the difference is statistically significant in the untreated control group).
Figure 3
Increasing the time of treatment with β-elemene decreases glioblastoma cells viability. The 5000 cells per well were sown in 96-well plates. Cell lines U251 and U118 were treated with 50 μg/mL β-elemene and cell lines U87 and A172 were treated with 60 μg/ mL β-elemene for 0, 24, 48, 72, 96, 120 and 144 hours (A-D). The CCK-8 was utilized to determine inhibitory effect of β-elemene on the proliferation of the cells in different time intervals. The results are shown as mean ± SD of the three experiments (p <0.05, the difference is statistically significant in the untreated control group).
Figure 4
Migration of human glioblastoma cell lines U251, U118, A172 and U87 were inhibited by β-elemene. In this wound healing assay, 5000 cells/well were sown into 6-well plates, cultured and photographed at the time intervals of 12, 24, 36 and 48 hours in at least three independent groups (β-elemene treated vs. control groups). The data were analyzed as mean ± SD and p <0.05. The human glioblastoma cells treated with β-elemene was found to have much lower speed moving to the gaps compared to the untreated control group cells (A-D).
Figure 5
β-Elemene suppresses U251 cell tumorigenicity in vivo. Five- to six-week old female nude mice were injected subcutaneously with (1 × 107) U251 cells and the tumor weights from the β-elemene-treated group and control group (untreated group) were measured at 28 days post-injection (A).The tumorigenicity of the U251 cells was remarkably reduced in the group that was treated with β-elemene as compared to the group that was not treated with β-elemene (p <0.05) (B). Immunohistochemistry staining of RNF135 of the tumors treated with β-elemene and not treated with β-elemene (control group), original magnification ×400, ×100 (C).
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