scholarly journals The enzyme L-isoaspartyl (D-aspartyl) methyltransferase promotes migration and invasion in human U-87 MG and U-251 MG glioblastoma cell lines

2021 ◽  
Vol 140 ◽  
pp. 111766
Author(s):  
Fatima Belkourchia ◽  
Richard R. Desrosiers
2019 ◽  
Author(s):  
jiang yongan ◽  
Liu Jia yu ◽  
Hong Wangwang ◽  
Fei Xiaowei ◽  
Liu ru'en

Abstract Arctigenin (ARG) is a natural lignan compound extracted from arctium lappa and has displayed anticancer functions and effective treatments in a variety of cancers.Studies had shown that Arctigenin(ARG) inhibits tumors through the AKT/MTOR pathway and mediates autophagy.However,the role in glioma cellshave not still fully understood.This study was designed to investigate whether Arctigenin(ARG) can mediateAKT/mTOR pathway in glioma to regulate autophagy,and affected glioma cells growth and survival.We found that the dose-dependent downregulation of Arctigenin(ARG),reducing cell proliferation,migration and invasion in two human glioblastoma cell lines (U87, T98G),These phenomena were reversed after the administration of the AKT agonist (SC79). Arctigenin(ARG) also affected other autophagy markers such as p62, LC3B.In addition, the apoptotic molecules cleaved-PARP,caspase-9, and cleaved-caspase3 were also dose-dependently altered.


2012 ◽  
Vol 318 (15) ◽  
pp. 1901-1912 ◽  
Author(s):  
Maria Grazia Cattaneo ◽  
Elisa Cappellini ◽  
Lucia M. Vicentini

2018 ◽  
Vol 2018 ◽  
pp. 1-11
Author(s):  
Wen Song ◽  
Zhenling Wang ◽  
Pengcheng Kan ◽  
Zhuolin Ma ◽  
Yaru Wang ◽  
...  

Background. BCL6 was a critical prooncogene of human B-cell lymphomas which promoted tumor progress and contributed to malignant behavior in several kinds of cancers. This study was to detect the expression of BCL6 and its biological effect on glioma. Methods. RT-PCR and Western blot were used to detect the expression of BCL6 mRNA and protein in tissues and glioblastoma cell lines. The expression of BCL6 was knockdown in two glioblastoma cell lines (U87 and U251) using BCL6 shRNA. The CCK8, colony-formation, flow cytometry, Transwell, and wound-healing assays were used to evaluate the malignant phenotypic change of glioblastoma cells. Results. The expression of BCL6 was higher in glioma tissues and glioblastoma cell lines than normal tissues. Knockdown of BCL6 expression reduced the proliferation, migration, and invasion of glioblastoma cells. Moreover, knockdown of BCL6 changed expression of proteins related to malignant behaviors of glioblastoma cells. The suppression of BCL6 could increase chemosensitivity of U87 and U251 to temozolomide. Downregulation of BCL6 levels suppressed the expression of BCL2, cyclin D1, MMP2, and MMP9 proteins as well as two classic signaling pathway proteins p-AKT and p-ERK. Simultaneously, BAX and p21 protein levels were upregulated along with knockdown of BCL6. Conclusions. Our results indicated that BCL6 may be a tumor oncogene involved in the progression of glioma via affecting AKT and MAPK signaling pathways.


2018 ◽  
Vol 32 (2) ◽  
pp. 230-239 ◽  
Author(s):  
Mihaela Aldea ◽  
Ioan Stefan Florian ◽  
Monica Potara ◽  
Olga Soritau ◽  
Timea Nagy-Simon ◽  
...  

Abstract Introduction: Metformin (MET), an old anti-diabetic drug, has proven unexpected anti-glioblastoma effects, by impacting cell proliferation, migration and invasion. However, its remarkable anti-cancer efficacy is mainly limited to the use of high millimolar concentrations in in vitro studies, which are hard to be attained in the clinical setting. Aim: The aim of this paper was to synthetize gold nanoparticles loaded with MET and to test if an enhanced drug delivery via nanotechnology could overcome the limitations of small drug concentrations. Materials and Methods: Gold nanoparticles were functionalized with chitosan (GNPc) and loaded with 80 μM of MET. Their size, zeta potential and stability were characterized and their internalization within tumor cells was assayed through dark field microscopy. Three primary glioblastoma stem cell lines were treated with 5, 10 and 20 μg/mL concentrations of nanoparticles and irradiated. The anti-tumoral effect was evaluated through the MTT cell viability assay. Results: MET-GNPc are easily synthetized and have a positive zeta potential, spherical shape and a median size of 26 nm. MET-GNPc have an increased cell internalization and affect the viability of all three glioblastoma cell lines used compared to control and free MET. However, their anti-cancer effect is not statistically different when compared to GNPc, although a slight tendency to a better response may be observed. Conclusion:Despite an increased cell internalization, the small micromolar concentrations of metformin does not bring an additional benefit to chitosan-based GNPs. Novel delivery methods being able to carry a higher drug concentration of metformin should be tested.


2020 ◽  
Vol Volume 13 ◽  
pp. 8813-8823 ◽  
Author(s):  
Dulce Carolina Rodríguez-Lozano ◽  
Diana Elisa Velázquez-Vázquez ◽  
Aylin Del Moral-Morales ◽  
Ignacio Camacho-Arroyo

1996 ◽  
Vol 102 (1-2) ◽  
pp. 57-63 ◽  
Author(s):  
Shravan Kumar Chintala ◽  
Raymond Sawaya ◽  
Ziya Levent Gokaslan ◽  
Jasti Sambasiva Rao

2020 ◽  
Vol 104 (3-4) ◽  
pp. 90-98 ◽  
Author(s):  
Chih-Hui Chang ◽  
Hung-Pei Tsai ◽  
Shih-Hsun Kuo ◽  
Joon-Khim Loh ◽  
Chien-Ju Lin ◽  
...  

Objectives: We determined the anticancer potency of CDDO-Me in glioblastoma cell lines and the underlying mechanisms in vitro. Summary: CDDO-Me is a synthetic triterpenoid with more potent anticancer and cancer preventive actions compared with the original triterpenoid CDDO. Methods: Two glioblastoma cell lines, GBM8401 and GBM8901, were utilized to test the effect of CDDO-Me on cell viability, cell migration, and cell invasion using the MTT, wound healing, and transwell migration assays, respectively. Additionally, Western blotting was used to determine the protein expression levels of N-cadherin, cyclin D1, and vascular endothelial growth factor. Results: At nanomolar concentrations, CDDO-Me inhibited proliferation, migration, and invasion in both cell lines. In addition, CDDO-Me exhibited a dose-dependent downregulation in the protein levels of N-cadherin, cyclin D1, and vascular endothelial growth factor in GBM8401 and GBM8901 cells. Conclusions: CDDO-Me exhibited anticancer effects at low nanomolar concentrations and should be considered as a potential chemotherapeutic agent for glioblastoma.


Sign in / Sign up

Export Citation Format

Share Document