Limonin attenuates the stemness of breast cancer cells via suppressing MIR216A methylation

Zhou, Shu; Wang, Caihong; Chang, Deyu; Zhu, Xiuna; Sai, Chunmei; Pei, Jian

doi:10.1016/j.biopha.2019.108699

Cited by 42 publications

(28 citation statements)

References 22 publications

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“…Microenvironmental stress has been shown to promote the enrichment of cells with stemness . TRIB3 is an important stress‐related gene, which can be induced and upregulated by various stimuli and participate in cell apoptosis, blood sugar and lipid metabolism, adipocyte differentiation, cell stress, and other processes; this hints that TRIB3 could affect CSC progression. For example, a recent work indicates that TRIB3 could increase colorectal cancer cell stemness .…”

Section: Discussionmentioning

confidence: 99%

TRIB3 confers glioma cell stemness via interacting with β‐catenin

Chen

et al. 2020

Environmental Toxicology

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Here, we aim to explore whether tribbles pseudokinase 3 (TRIB3) enhances glioma cell stemness. TRIB3 was overexpressed in glioma tissues and cell-formed spheres, positively correlated with the size and grade. Additionally, TRIB3 expression displayed a negative correlation with the overall survival rate of glioma patients. Moreover, TRIB3 knockdown reduced the stemness of nonadherent spheres, evident by the decreased sphere-forming ability, stemness master expression, and ALDH1 activity, while TRIB3 overexpression enhanced the stemness of adherent cells, which was rescued by β-catenin knockdown. Mechanistically, TRIB3 activated β-catenin signaling via physically interacting with β-catenin. This study suggests that the TRIB3-β-catenin interaction is responsible for glioma cell stemness. K E Y W O R D Sβ-catenin, glioma, stemness, TRIB3, Wnt

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Section: Discussionmentioning

confidence: 99%

TRIB3 confers glioma cell stemness via interacting with β‐catenin

Chen

et al. 2020

Environmental Toxicology

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“…MethPrimer ( http://www.urogene.org/cgi-bin/methprimer/methprimer.cgi ) was used to analyze the CpG islands on Sox2, Oct4, and Nanog promoter using the method previously published [15]. Briefly, the PureLink™ Pro 96 Genomic DNA Purification Kit (Thermo Fisher Scientific) was used to extract genomic DNA.…”

Section: Methodsmentioning

confidence: 99%

The Na+/K+ ATPase Inhibitor Ouabain Attenuates Stemness and Chemoresistance of Osteosarcoma Cells

et al. 2019

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Departmental sources Background: The purpose of this study was to explore the effects of the Na+/K+ ATPase inhibitor ouabain in regulating osteosarcoma (OS) cell stemness. Material/Methods: Western blot, qPCR, sphere-forming analysis, DNA methylation analysis, and Ca 2+ concentration detection were performed to evaluate the stem-like traits of cells and ouabain-induced effects and related mechanisms on OS cell stemness. Cell viability assessment was performed to evaluate the effect of ouabain on OS cell chemosensitivity. Results: Ouabain reduced the ALDH1 activity, the expression of critical stemness regulators, sphere size and number, and migration, invasion, and adhesion ability, but had little effects on cell viability. Additionally, the intracellular Ca 2+ concentration and methylation level of the critical stemness regulators were higher in OS cells than in spheres formed by OS cells. Mechanistic studies revealed that ouabain leads to DNA methylation of stemness markers through increasing intracellular Ca 2+ concentration. Notably, inhibition of Ca 2+ channel or DNA methylation rescued the inhibition of ouabain on OS cell stemness. Additionally, ouabain enhances cisplatin sensitivity of OS cells, which is involved in Ca 2+ channel and DNA methylation. Conclusions: This work provides a potential compound for treating OS patients, especially OS patients with chemoresistance.

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“…[20][21][22] The Wnt/β-catenin signaling pathway is commonly hyperactivated in CSCs. [23][24][25] HBX has been recognized as a critical element of Wnt signaling activation and enhances the stabilization of β-catenin to boost Wnt/β-catenin signaling. 26,27 However, the mechanism by which HBX promotes Wnt signaling activation has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Silencing MYH9 blocks HBx-induced GSK3β ubiquitination and degradation to inhibit tumor stemness in hepatocellular carcinoma

Lin

et al. 2020

Sig Transduct Target Ther

133

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MYH9 has dual functions in tumors. However, its role in inducing tumor stemness in hepatocellular carcinoma (HCC) is not yet determined. Here, we found that MYH9 is an effective promoter of tumor stemness that facilitates hepatocellular carcinoma pathogenesis. Importantly, targeting MYH9 remarkably improved the survival of hepatocellular carcinoma-bearing mice and promoted sorafenib sensitivity of hepatocellular carcinoma cells in vivo. Mechanistic analysis suggested that MYH9 interacted with GSK3β and reduced its protein expression by ubiquitin-mediated degradation, which therefore dysregulated the β-catenin destruction complex and induced the downstream tumor stemness phenotype, epithelial-mesenchymal transition, and c-Jun signaling in HCC. C-Jun transcriptionally stimulated MYH9 expression and formed an MYH9/GSK3β/β-catenin/c-Jun feedback loop. X protein is a hepatitis B virus (HBV)-encoded key oncogenic protein that promotes HCC pathogenesis. Interestingly, we observed that HBV X protein (HBX) interacted with MYH9 and induced its expression by modulating GSK3β/β-catenin/c-Jun signaling. Targeting MYH9 blocked HBX-induced GSK3β ubiquitination to activate the β-catenin destruction complex and suppressed cancer stemness and EMT. Based on TCGA database analysis, MYH9 was found to be elevated and conferred poor prognosis for hepatocellular carcinoma patients. In clinical samples, high MYH9 expression levels predicted poor prognosis of hepatocellular carcinoma patients. These findings identify the suppression of MYH9 as an alternative approach for the effective eradication of CSC properties to inhibit cancer migration, invasion, growth, and sorafenib resistance in HCC patients. Our study demonstrated that MYH9 is a crucial therapeutic target in HCC.

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Limonin attenuates the stemness of breast cancer cells via suppressing MIR216A methylation

Cited by 42 publications

References 22 publications

TRIB3 confers glioma cell stemness via interacting with β‐catenin

TRIB3 confers glioma cell stemness via interacting with β‐catenin

The Na+/K+ ATPase Inhibitor Ouabain Attenuates Stemness and Chemoresistance of Osteosarcoma Cells

Silencing MYH9 blocks HBx-induced GSK3β ubiquitination and degradation to inhibit tumor stemness in hepatocellular carcinoma

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