Chrysin suppresses proliferation, migration, and invasion in glioblastoma cell lines via mediating the ERK/Nrf2 signaling pathway

Background: Sulfiredoxin (Srx) has been identified to play important roles in the development of various cancers. However, the precise effects and underlying mechanism of Srx on the progression of HCC are far from being fully understood. Materials and Methods: The abundances of Srx in THLE-2 cell and HCC cell lines were determined by western blot and RT-qPCR. Next, SK-Hep-1 cells were transfected with shRNA-Srx or shRNA-NC and treated with TBHQ (an extracellular signal-regulated kinase (ERK) activator) for functional experiments. Then, CCK8 and colony formation assays were used to determine cell proliferation and clone-forming abilities in vitro. Cell migration and invasion were assessed via wound healing and transwell assays. The expression of MMP2, MMP9 and key members in ERK/nuclear factor E2 related factor (Nrf2) signaling pathway was detected by performing western blot analysis. Results: We reported evidence that Srx was frequently up-regulated in HCC cell lines. Srx interference constrained cell proliferation, colony formation rate, migration and invasion of SK-Hep-1 cells. Moreover, mechanistic investigations indicated that Srx interference significantly inhibited the activation of ERK/Nrf2 signaling pathway, and ERK activator TBHQ can reverse the functions of Srx interference in SK-Hep-1 cells. Conclusion: Overall, Downregulation of Srx might impede HCC progression by suppressing ERK/Nrf2 signaling pathway. Findings in the current study reported the functional involvement and molecular mechanism of Srx in HCC, suggesting that Srx might have a potential therapeutic value in HCC treatment.

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Arctigenin upregulates apoptosis through the AKT/MTOR pathway, inhibiting the proliferation of glioma

10.21203/rs.2.18701/v1 ◽

2019 ◽

Author(s):

jiang yongan ◽

Liu Jia yu ◽

Hong Wangwang ◽

Fei Xiaowei ◽

Liu ru'en

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Glioma Cells ◽

Mtor Pathway ◽

Migration And Invasion ◽

Glioblastoma Cell ◽

Caspase 9 ◽

Arctium Lappa ◽

Dose Dependent ◽

Glioblastoma Cell Lines

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.

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Silencing of Eps8 blocks migration and invasion in human glioblastoma cell lines

Experimental Cell Research ◽

10.1016/j.yexcr.2012.05.010 ◽

2012 ◽

Vol 318 (15) ◽

pp. 1901-1912 ◽

Cited By ~ 12

Author(s):

Maria Grazia Cattaneo ◽

Elisa Cappellini ◽

Lucia M. Vicentini

Keyword(s):

Cell Lines ◽

Migration And Invasion ◽

Glioblastoma Cell ◽

Human Glioblastoma ◽

Human Glioblastoma Cell ◽

Glioblastoma Cell Lines

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Differential sensitivities of glioblastoma cell lines towards metabolic and signaling pathway inhibitions

Cancer Letters ◽

10.1016/j.canlet.2013.03.020 ◽

2013 ◽

Vol 336 (2) ◽

pp. 299-306 ◽

Cited By ~ 17

Author(s):

Colin R. Kennedy ◽

Sarah B. Tilkens ◽

Hong Guan ◽

Justine A. Garner ◽

Penelope M.Y. Or ◽

...

Keyword(s):

Signaling Pathway ◽

Cell Lines ◽

Glioblastoma Cell ◽

Glioblastoma Cell Lines

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miR-548x and miR-4698 controlled cell proliferation by affecting the PI3K/AKT signaling pathway in Glioblastoma cell lines

Scientific Reports ◽

10.1038/s41598-020-57588-5 ◽

2020 ◽

Vol 10 (1) ◽

Cited By ~ 3

Author(s):

Mohammad Reza kalhori ◽

Ehsan Arefian ◽

Fereshteh Fallah Atanaki ◽

Kaveh Kavousi ◽

Masoud Soleimani

Keyword(s):

Cell Proliferation ◽

Signaling Pathway ◽

Cell Lines ◽

Akt Signaling ◽

Glioblastoma Cell ◽

Akt Signaling Pathway ◽

Glioblastoma Cell Lines

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Knockdown of BCL6 Inhibited Malignant Phenotype and Enhanced Sensitivity of Glioblastoma Cells to TMZ through AKT Pathway

BioMed Research International ◽

10.1155/2018/6953506 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11

Author(s):

Wen Song ◽

Zhenling Wang ◽

Pengcheng Kan ◽

Zhuolin Ma ◽

Yaru Wang ◽

...

Keyword(s):

Cell Lines ◽

Mapk Signaling ◽

Migration And Invasion ◽

Phenotypic Change ◽

Glioblastoma Cell ◽

Glioblastoma Cells ◽

Protein Levels ◽

Normal Tissues ◽

Enhanced Sensitivity ◽

Glioblastoma Cell Lines

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.

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