Effect of Bmi-1-mediated NF-κB signaling pathway on the stem-like properties of CD133+ human liver cancer cells

Ma, Dawei; Zhang, Yinhua; Ding, Deping; Li, Juan; Chen, Linli; Tian, You-You; Ao, Kang-Jian

doi:10.3233/cbm-181329

Cited by 16 publications

(12 citation statements)

References 36 publications

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“…Because the lack of p16Ink4a, the retinoblastoma product (pRB) can be phosphorylated by the cyclin D/Cdk4/6 complex, which allows the transcription factor (E2F)-dependent transcription that leads to the progression of cell cycle and synthesis of DNA. Ma et al ( 27 ) found that Bmi - 1 may play an important role in the progression of liver cancer by the independent pathway of p16Ink4a to regulate the cell multiplication. Furthermore, murine double minute 2 (MDM2)-mediated p53 degradation causes low p53 levels in the absence of p19Arf, thus could prevent cell cycle arrest and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Expression and correlation of Bmi-1, AEG-1 and FHIT in bladder transitional cell carcinoma

Su¹,

Li²,

Li³

2020

Transl Cancer Res TCR

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Background: To explore the expression and correlation of B-cell-specific Moloney murine leukemia virus insertion site 1 (Bmi-1), astrocyte elevated gene-1 (AEG-1) and fragile histidine triad (FHIT) in bladder transitional cell carcinoma (BTCC).Methods: Forty-six tissue samples were obtained from patients diagnosed with primary bladder cancer during the first radical cystectomy between June 2010 and January 2014. The expression of Bmi-1, AEG-1 and FHIT in normal tissues and BTCC tissues in different histological cell types, clinical pathological stages and lymph node metastatic status were evaluated by quantitative real time polymerase chain reaction (qRT-PCR), Western blot and immunohistochemistry. Relationships between Bmi-1, AEG-1 and FHIT were determined using linear correlation coefficient. Results:The results of qRT-PCR showed the relative expression of Bmi-1 and AEG-1 were higher and the expression of FHIT was lower in BTCC tissues than those in normal tissues, whether in different histological cell types, clinical pathological stages or lymph node metastatic status (P<0.05). Similarly, the up-regulated expression of Bmi-1 and AEG-1 and down-regulated expression of FHIT in BTCC tissues were observed by the Western blot and immunohistochemistry compared with normal tissues (P<0.05). Linear correlation analysis showed the expression of Bmi-1 was positively correlated with AEG-1 (r>0.90, P<0.01), which was negatively correlated with the expression of FHIT, respectively (r=−0.84, P<0.05). Conclusions:The study demonstrated the up-regulated expression of Bmi-1 and AEG-1 and the downregulated expression of FHIT in BTCC tissues. The interaction of Bmi-1, AEG-1 and FHIT may involve in the tumorigenesis, progression and invasion of BTCC through NF-κB/MMP-9 pathway.

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Section: Discussionmentioning

confidence: 99%

Expression and correlation of Bmi-1, AEG-1 and FHIT in bladder transitional cell carcinoma

Su¹,

Li²,

Li³

2020

Transl Cancer Res TCR

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“…Furthermore, we investigated the role of G-Rg1 in the regulation of NF- κ B activity. Previous studies have indicated that NF- κ B regulates the release of proinflammatory cytokines, and the blockade of NF- κ B activation can decrease the expression of proinflammatory factors [36, 37]. Gao et al also demonstrated that G-Rg1 inhibited inflammation effectively through the inhibition of glucocorticoid receptor-dependent NF- κ B activity [38].…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 Ameliorates Palmitic Acid-Induced Hepatic Steatosis and Inflammation in HepG2 Cells via the AMPK/NF-κB Pathway

Xiao

Zhang

Yang

et al. 2019

International Journal of Endocrinology

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Nonalcoholic fatty liver disease (NAFLD) is one of the common diseases in the world, and it can progress from simple lipid accumulation to sustained inflammation. The present study was designed to investigate the effects and underlying mechanisms of ginsenoside Rg1 (G-Rg1) treatment on NAFLD in vitro. HepG2 cells were treated with palmitic acid (PA) to induce steatosis and inflammation and then successively incubated with G-Rg1. Lipids accumulation was analyzed by Oil Red O staining and intracellular triglyceride (TG) quantification. Inflammatory conditions were examined by quantifying the levels of cell supernatant alanine transaminase/aspartate aminotransferase (ALT/AST) and secretory proinflammatory cytokines, including IL-1β, IL-6, and TNF-α in the cell supernatants. Quantitative RT-PCR and western blotting were used to measure the expressions of genes and proteins associated with lipogenic synthesis and inflammation, including AMP-activated protein kinase (AMPK) and nuclear factor-kappa B (NF-κB) pathways. HepG2 cells were pretreated with an AMPK inhibitor; then, Oil Red O staining and TG quantification were performed to study the lipid deposition. Phospho-AMPK (Thr172) (p-AMPK) and phospho-acetyl-CoA carboxylase (Ser79) (p-ACCα) were quantified by immunoblotting. Immunofluorescence was performed to demonstrate the nuclear translocation of NF-κB P65. The present study showed that PA markedly increased the intracellular lipid droplets accumulation and TG levels, but decreased AMPK phosphorylation and the expressions of its downstream lipogenic genes. However, G-Rg1 alleviated hepatic steatosis and reduced the intracellular TG content; these changes were accompanied by the activation of the AMPK pathway. In addition, blocking AMPK by using the AMPK inhibitor markedly abolished the G-Rg1-mediated protection against PA-induced lipid deposition in HepG2 cells. Furthermore, G-Rg1 reduced the ALT/AST levels and proinflammatory cytokines release, which were all enhanced by PA. These effects were correlated with the inactivation of the NF-κB pathway and translocation of P65 from the cytoplasm to the nucleus. Overall, these results suggest that G-Rg1 effectively ameliorates hepatic steatosis and inflammation, which might be associated with the AMPK/NF-κB pathway.

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“…Published articles have shown that CSCs are the main factor in uencing tumor recurrence after treatment and that activation of some protooncogenes in CSCs, such as PCGF4, cause tumor recurrence [7,8]. Moreover, PCGF4 has a key role in EMT (the epithelial-mesenchymal transition), cancer stem cells, and chemotherapy resistance [9][10][11][12][13][14][15][16][17][18]. In head and neck squamous cell carcinoma, PCGF4 + CSCs show cisplatin resistance, with possible relapse after chemotherapy [9].…”

Section: Introductionmentioning

confidence: 99%

PCGF2 and PCGF4 Oppositely Drive Stem-like Properties in Hepatocellular Carcinoma

Zhou

Feng

et al. 2022

Preprint

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Background: PCGF4 as a cancer stem cells (CSC) marker displays stem cell-like properties, and drug resistance in hepatocellular carcinoma (HCC). PCGF2, a homologue of PCGF4, the effect of PCGF2 on liver CSCs (LCSCs) and drug resistance and the molecular mechanism of this effect have not been documented.Methods: To measure the cell viability, CSCs properties of the cells, the Cell Counting Kit-8, spheroid assay, and flow cytometry assays were applied in the HCC cell lines, respectively. The self-renewal was determined by limiting dilution assay. Also, IHC and western blotting were used to detect protein expression of PCGF2 and PCGF4 in human HCC tissues, cell lines and the effects of PCGF2 overexpression on the p38 MAPK genes expression. Kaplan-Meier curves were generated for overall survival (OS) and disease-free survival (DFS). We performed KEGG analysis on target genes through the R language cluster profiler package.Results: IHC showed that expression of PCGF4 and PCGF2 correlate inversely in HCC cell lines and HCC tumors. Overexpression of PCGF2 inhibited the stemness of HCC cells refected by decreasing sphere-forming and self-renewal capacities as well as the expression of CSCs markers. Interestingly, down-regulating PCGF4 led to similar results as up-regulating PCGF2. We also found that PCGF2 and PCGF4 oppositely regulated the stem-like properties driven by the p38 MAPK signalling pathway.Conclusion: Our results suggest that PCGF2 inhibits the stem cell population, reduces the sphere formation ability in HCC cell lines, and increases sensitivity to sorafenib by targeting p38 MAPK signalling.

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Effect of Bmi-1-mediated NF-κB signaling pathway on the stem-like properties of CD133+ human liver cancer cells

Abstract: Down-regulating Bmi-1 may inhibit the biological properties of CD133+ LCSC by blocking NF-κB signaling pathway, which lays a scientific foundation for the clinical treatment of liver cancer.

Cited by 16 publications

References 36 publications

Expression and correlation of Bmi-1, AEG-1 and FHIT in bladder transitional cell carcinoma

Expression and correlation of Bmi-1, AEG-1 and FHIT in bladder transitional cell carcinoma

Ginsenoside Rg1 Ameliorates Palmitic Acid-Induced Hepatic Steatosis and Inflammation in HepG2 Cells via the AMPK/NF-κB Pathway

PCGF2 and PCGF4 Oppositely Drive Stem-like Properties in Hepatocellular Carcinoma

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