Retinol dehydrogenase-10 promotes development and progression of human glioma via the TWEAK-NF-κB axis

Guan, Feng; Wang, Liang; Hao, Shuyu; Wu, Zhen; Bai, Jian; Kang, Zhuang; Zhou, Quan; Chang, Hong; Yin, Hui; Li, Da; Tian, Kaibin; Ma, Junpeng; Zhang, Guijun; Zhang, Junting

doi:10.18632/oncotarget.22166

Cited by 8 publications

(6 citation statements)

References 50 publications

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“…For instance, NAMPT can be secreted from microglia, 73 and its inhibitor can prolong GBM‐bearing animals' survival time on accompany by PD‐1 checkpoint blockade. 74 TNFSF12‐TNFRSF12A can modulate glioma progression 75 , 76 and may participate in microglia activation. 77 GDF2‐ACVRL1 can modulate glioma angiogenesis, 78 but its association with microglia was elusive.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of pyroptosis‐related gene signatures for glioblastoma immune microenvironment and target therapy

et al. 2023

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Glioblastoma (GBM) is a malignant brain tumour, but its subtypes (mesenchymal, classical, and proneural) show different prognoses. Pyroptosis is a programmed cell death relating to tumour progression, but its association with GBM is poorly understood. In this work, we collected 73 GBM samples (the Xiangya GBM cohort) and reported that pyroptosis involves tumour‐microglia interaction and tumour response to interferon‐gamma. GBM samples were grouped into different subtypes, cluster 1 and cluster 2, based on pyroptosis‐related genes. Cluster 1 samples manifested a worse prognosis and had a more complicated immune landscape than cluster 2 samples. Single‐cell RNA‐seq data analysis supported that cluster 1 samples respond to interferon‐gamma more actively. Moreover, the machine learning algorithm screened several potential compounds, including nutlin‐3, for cluster 1 samples as a novel treatment. In vitro experiments supported that cluster 1 cell line, T98G, is more sensitive to nutlin‐3 than cluster 2 cell line, LN229. Nutlin‐3 can trigger oxidative stress by increasing DHCR24 expression. Moreover, pyroptosis‐resistant genes were upregulated in LN229, which may participate against nutlin‐3. Therefore, we hypothesis that GBM may be able to upregulate pyroptosis resistant related genes to against nutlin‐3‐triggered cell death. In summary, we conclude that pyroptosis highly associates with GBM progression, tumour immune landscape, and tumour response to nutlin‐3.

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Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of pyroptosis‐related gene signatures for glioblastoma immune microenvironment and target therapy

et al. 2023

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“…DR3 is an important receptor of TWEAK, [15] and TWEAK can activate DR3 to promote NF-κB activation. [16,17] signal protein of TWEAK. [18,19] Research has suggested that TWEAK can directly induce NF-κB activation, while the activated NF-κB can promote angiogenesis and induce cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

TWEAK promotes inflammatory response in liver fibrosis

Kong,

Yang,

et al. 2023

J Biochem & Molecular Tox

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This study aimed to investigate the role and mechanism of tumor necrosis factor‐like weak inducer of apoptosis (TWEAK) in liver fibrosis. The liver Kupffer cells (KCs) and mononuclear macrophages (J774A.1) were used as the objects of study to induce M1 polarization with LPS/IFN‐γ. After TWEAK intervention, the M1 cell proportion and marker cytokine levels were detected. Thereafter, CD266 expression was silenced, and NLRP3 expression was inhibited by the NLRP3 inhibitor, so as to investigate the impact of TWEAK on M1 polarization of KCs. In addition, the mouse model of liver fibrosis was constructed to observe the influence of TWEAK on mouse liver fibrosis. According to our results, TWEAK promoted M1 polarization of liver KCs and J774A.1 cells, and silencing CD266 expression or treatment with the NLRP3 inhibitor suppressed the effect of TWEAK. In the mouse experiment, it was discovered that after knocking down NLRP3 expression or using NLRP3 inhibitor to antagonize the effect of TWEAK, the mouse liver function and M1 cell level in liver tissues were improved.

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“…Additionally, we found that RDH10 knockdown suppressed the invasion of glioma cells. [13] However, the role of RDH10 in the migration and invasion in glioma cells requires further investigation. In this study, we confirmed that RDH10 was highly expressed in glioma cells, and downregulation of RDH10 inhibited the invasion of glioma cells.…”

Section: Discussionmentioning

confidence: 99%

Retinol dehydrogenase 10 promotes metastasis of glioma cells via the transforming growth factor-β/SMAD signaling pathway

Guan

Kang

Wang

et al. 2019

Chinese Medical Journal

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Background:Glioma is the most common primary malignant tumor in the central nervous system. Because of the resistance of glioma to chemoradiotherapy and its aggressive growth, the survival rate of patients with glioma has not improved. This study aimed to disclose the effect of retinol dehydrogenase 10 (RDH10) on the migration and invasion of glioma cells, and to explore the potential mechanism.Methods:Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the expression levels of RDH10 in healthy glial cells and glioma cells. Human glioma cell strains, U87 and U251, were infected with negative control or RDH10-interfering lentiviruses. RT-PCR and Western blotting were performed to determine the knockdown efficiency. Scratch and transwell assays were used to assess cell migration and invasion after RDH10 knockdown. Finally, changes in transforming growth factor-β (TGF-β)/SMAD signaling pathway-related expression were examined by Western blotting. Differences between groups were analyzed by one-way analysis of variance.Results:RDH10 was highly expressed in glioma cells. Compared with the control group, RDH10 knockdown significantly reduced RDH10 messenger RNA and protein expression levels in U87 and U251 glioma cells (U87: 1.00 ± 0.08 vs. 0.22 ± 0.02, t = 16.55, P < 0.001; U251: 1.00 ± 0.17 vs. 0.39 ± 0.01, t = 6.30, P < 0.001). The scratch assay indicated that compared with the control group, RDH10 knockdown significantly inhibited the migration of glioma cells (U87: 1.00% ± 0.04% vs. 2.00% ± 0.25%, t = 6.08, P < 0.01; U251: 1.00% ± 0.11% vs. 2.48% ± 0.31%, t = 5.79, P < 0.01). Furthermore, RDH10 knockdown significantly inhibited the invasive capacity of glioma cells (U87: 97.30 ± 7.01 vs. 13.70 ± 0.58, t = 20.36, P < 0.001; U251: 96.20 ± 7.10 vs. 18.30 ± 2.08, t = 18.51, P < 0.001). Finally, Western blotting demonstrated that compared with the control group, downregulation of RDH10 significantly inhibited TGF-β expression, phosphorylated SMAD2, and phosphorylated SMAD3 (TGF-β: 1.00 ± 0.10 vs. 0.53 ± 0.06, t = 7.05, P < 0.01; phosphorylated SMAD2: 1.00 ± 0.20 vs. 0.42 ± 0.17, t = 4.01, P < 0.01; phosphorylated SMAD3: 1.00 ± 0.18 vs. 0.41 ± 0.12, t = 4.12, P < 0.01).Conclusion:RDH10 knockdown might inhibit metastasis of glioma cells via the TGF-β/SMAD signaling pathway.

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Retinol dehydrogenase-10 promotes development and progression of human glioma via the TWEAK-NF-κB axis

Cited by 8 publications

References 50 publications

Comprehensive analysis of pyroptosis‐related gene signatures for glioblastoma immune microenvironment and target therapy

Comprehensive analysis of pyroptosis‐related gene signatures for glioblastoma immune microenvironment and target therapy

TWEAK promotes inflammatory response in liver fibrosis

Retinol dehydrogenase 10 promotes metastasis of glioma cells via the transforming growth factor-β/SMAD signaling pathway

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