Difference in the Inhibitory Effect of Temozolomide on TJ905 Glioma Cells and Stem Cells

Jin, Feng; Han, Guangkui; Zhang, Hao; Zhang, Ran; Li, Gen‐Hua; Feng, Song; Qin, Xianyun; Kong, Ling‐Bin; Nie, Qiang; Li, Huarong; Zhao, Lei

doi:10.3389/fneur.2017.00474

Cited by 4 publications

(5 citation statements)

References 27 publications

(27 reference statements)

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“…The results showed that TMZ effectively attenuated the duplication and cell cycle of glioma cells and stem cells in a dose‐dependent manner and had a greater effect on U87 cells and U251 cells, which revealed the presence of different resistant mechanism in glioma cells and glioma stem cells. Consistently, the suppressive effect of TMZ on TJ905 glioma cells was more significant than its effect on TJ905 stem cells . And Beier et al also discovered that glioblastoma stem cell had stronger resistance to TMZ compared with glioblastoma cells …”

Section: Discussionmentioning

confidence: 89%

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PLK1 inhibitor facilitates the suppressing effect of temozolomide on human brain glioma stem cells

Liu

Wang³

et al. 2018

J Cellular Molecular Medi

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Glioblastoma is the most frequent and most aggressive brain tumour in adults. Temozolomide is an oral chemotherapy drug and one of the major components of chemotherapy regimens used as a treatment of some brain cancers. We examined the tolerance of stem cells isolated from glioma cell line U87 and U251 to temozolomide (TMZ) and explored the effect of PLK1 (Polo like kinase 1) protein expression on TMZ sensibility. In our results, the inhibitory effects of TMZ on glioma cells U87, U251 and its stem cells were confirmed to be dose dependent and time dependent. Compared with glioma cells, the glioma stem cells showed a greater degree of tolerance. As the concentration of TMZ increased, the expression of PLK1 protein increased in U87 cells, CD133+ U87 stem cells and CD133‐ U87 cells. The increase range of PLK1 protein was large in CD133+ U87 stem cells and small in CD133‐ U87 cells. TMZ treatment in cells with low PLK1 protein expression efficiently suppressed the cell proliferation and sphere formation, while G2/M arrest was strongly induced. What's more, TMZ and PLK1 inhibitor synergize to inhibit glioma growth in vivo. In conclusion, our results suggest that down‐regulation of PLK1 protein enhanced the inhibition of TMZ on glioma stem cells, suggesting its clinical value to adverse TMZ resistance in glioma treatment.

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Section: Discussionmentioning

confidence: 89%

“…Consistently, the suppressive effect of TMZ on TJ905 glioma cells was more significant than its effect on TJ905 stem cells. 18 And Beier et al also discovered that glioblastoma stem cell had stronger resistance to TMZ compared with glioblastoma cells. 4 Relevant studies have revealed the PLK1 was involved in the mechanism of cancer growth.…”

Section: Discussionmentioning

confidence: 99%

PLK1 inhibitor facilitates the suppressing effect of temozolomide on human brain glioma stem cells

Liu

Wang³

et al. 2018

J Cellular Molecular Medi

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“…The procedure was carried out as previously described ( Jin et al, 2017 ). The total RNA was isolated from RAW264.7 cells or liver tissues using TRIzol reagent (Takara, Dalian, China).…”

Section: Methodsmentioning

confidence: 99%

Emodin Attenuates Lipopolysaccharide-Induced Acute Liver Injury via Inhibiting the TLR4 Signaling Pathway in vitro and in vivo

et al. 2018

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Aims: Emodin is an anthraquinone with potential anti-inflammatory properties. However, the possible molecular mechanisms and protective effects of emodin are not clear. The objective of this study was to investigate the possible molecular mechanisms and protective effects of emodin on lipopolysaccharide (LPS)-induced acute liver injury (ALI) via the Toll-like receptor 4 (TLR4) signaling pathway in the Raw264.7 cell line and in Balb/c mice.Methods: This study established an inflammatory cellular model and induced an ALI animal model. TLR4 was overexpressed by lentivirus and downregulated by small interfering RNA (siRNA) technology. The mRNA and protein levels of TLR4 and downstream molecules were detected in cells and liver tissue. The tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 levels in supernatant and serum were determined by ELISA. The distribution and expression of mannose receptor C type 1 (CD206) and arginase 1 (ARG1) in the liver were tested by immunofluorescence. Mouse liver function and histopathological observations were assessed.Results: Administration of emodin reduced the protein and/or mRNA levels of TLR4 and its downstream molecules following LPS challenge in Raw264.7 cells and in an animal model. Additionally, emodin suppressed the expression of TNF-α and IL-6 in cell culture supernatant and serum. The inhibitory effect of emodin was also confirmed in RAW264.7 cells, in which TLR4 was overexpressed or knocked down. Additionally, ARG1 and CD206 were elevated in the emodin groups. Emodin also decreased serum ALT and AST levels and alleviated the liver histopathological damage induced by LPS.Conclusion: Emodin showed excellent hepatoprotective effects against LPS-induced ALI, possibly by inhibiting TLR4 signaling pathways.

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“…The procedure was conducted as described previously by our group (Jin et al, 2017). Lentiviral vectors for TLR3 and a negative control were constructed by Tuojie (Wuhan, China).…”

Section: Methodsmentioning

confidence: 99%

Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis

Zhang

Liu

et al. 2019

Front. Mol. Neurosci.

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Herpes simplex encephalitis (HSE) is the most common infectious disease of the central nervous system worldwide. However, the pathogenesis of HSE is not clear. Research has shown that the immune response mediated by the toll-like receptor 3 (TLR3) signaling pathway is essential to protect the central nervous system against herpes simplex virus (HSV) infection. However, an excessive immune response may cause tissue damage accompanied by pathological changes. The aim of this study was to explore the molecular mechanism via which corilagin controls HSE through the TLR3 signaling pathway in vitro and in vivo . Cells and mice were pre-treated with polyriboinosinic polyribocytidylic acid [poly(I:C)] or HSV type 1, and then treated with corilagin. After treatment, the mRNA and protein levels of TLR3, TLR-like receptor-associated interferon factor (TRIF), tumor necrosis factor (TNF) receptor type 1-associated DEATH domain protein (TRADD), TNF receptor-associated factor (TRAF) 3 and 6, nuclear factor-kappa-B (NF-κB) essential modulator (NEMO), P38, and interferon regulatory factor 3 (IRF3) were decreased. Interleukin-6 (IL-6), TNF-α, and type 1 interferon-β were also decreased. When TLR3 expression was silenced or increased, corilagin still inhibited the expression of TLR3 and its downstream mediators. Hematoxylin-eosin (HE) staining and immunohistochemical examinations of mouse brain tissues revealed that corilagin lessened the degree of brain inflammation. Altogether, these results suggest that corilagin may regulate the immune response in HSE and relieve inflammatory injury by interfering with the TLR3 signaling pathway.

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Difference in the Inhibitory Effect of Temozolomide on TJ905 Glioma Cells and Stem Cells

Cited by 4 publications

References 27 publications

PLK1 inhibitor facilitates the suppressing effect of temozolomide on human brain glioma stem cells

PLK1 inhibitor facilitates the suppressing effect of temozolomide on human brain glioma stem cells

Emodin Attenuates Lipopolysaccharide-Induced Acute Liver Injury via Inhibiting the TLR4 Signaling Pathway in vitro and in vivo

Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis

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