Increased expression of CCAAT/enhancer binding protein β correlates with prognosis in glioma patients

Homma, Jumpei; Yamanaka, Ryuya; Yajima, Naoki; Tsuchiya, Naoto; Genkai, Nobuyuki; Sano, Masakazu; Tanaka, Ryuichi

doi:10.3892/or.15.3.595

Cited by 28 publications

(24 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other studies show that C/EBPβ and STAT3 can individually regulate glioma biology. For example, downregulation of C/EBPβ in glioma cells inhibited proliferation, invasion and tumorigenicity in mice (Aguilar-Morante, Cortes-Canteli, Sanz-Sancristobal, Santos, & Perez-Castillo, 2011; Homma et al, 2006), consistent with findings demonstrating that increased mRNA and protein levels of C/EBPβ are associated with a worse prognosis (Homma et al, 2006). Similarly, STAT3 is known to promote tumor growth in glioma.…”

Section: Proneural-to-mesenchymal Transition (Pmt) In Gliomasupporting

confidence: 80%

Glial Progenitors as Targets for Transformation in Glioma

Ilkhanizadeh¹,

Lau²,

Huang³

et al. 2014

Advances in Cancer Research

View full text Add to dashboard Cite

Glioma is the most common primary malignant brain tumor and arises throughout the central nervous system (CNS). Recent focus on stem-like glioma cells has implicated neural stem cells (NSCs), a minor precursor population restricted to germinal zones, as a potential source of gliomas. In this review, we will focus on the relationship between oligodendrocyte progenitor cells (OPCs), the largest population of cycling glial progenitors in the postnatal brain, and gliomas. Recent studies suggest that OPCs can give rise to gliomas. Furthermore, signaling pathways often associated with NSCs also play key roles during OPC lineage development. Recent advances suggesting that gliomas can undergo a switch from progenitor- to stem-like phenotype after therapy, implicating that an OPC-origin is more likely than previously recognized. Future in-depth studies of OPC biology may shed light on the etiology of OPC-derived gliomas and reveal new therapeutic avenues.

show abstract

Section: Proneural-to-mesenchymal Transition (Pmt) In Gliomasupporting

confidence: 80%

Glial Progenitors as Targets for Transformation in Glioma

Ilkhanizadeh¹,

Lau²,

Huang³

et al. 2014

Advances in Cancer Research

View full text Add to dashboard Cite

show abstract

“…Emerging evidence has shown that C/EBPb exists in three isoforms: LAP1, LAP2 and LIP, and that dysregulation of C/EBPb is markedly correlated with malignancy of several tumors, including glioma, Wilms tumors, renal cell carcinoma and ovarian tumor (Homma et al, 2006;Li et al, 2005;Oya et al, 2003;Sundfeldt et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Shan

Xiong

et al. 2014

Journal of Cell Science

View full text Add to dashboard Cite

Epithelial-mesenchymal transition (EMT) is a developmental program that is associated with esophageal squamous cell carcinoma (ESCC) progression and metastasis. Recently, C/EBPb has been reported to be an EMT inducer in cancer. However, the detailed molecular mechanisms remain unclear. Here, we report for the first time, that the truncated CCAAT-enhancer-binding protein b (C/EBPb) LIP isoform is abnormally overexpressed and correlated with cancer metastasis in clinical specimens of human ESCC. Furthermore, we demonstrate that C/EBPb LIP mediates epithelial growth factor (EGF)-induced EMT and increases migration and invasion of esophageal cancer cells in a manner that is dependent on miR-203 inactivation. Finally, we identified miR-203 as a direct target of C/EBPb LIP. Disruption of C/EBPb LIP attenuated the EGF-mediated decrease in miR-203, whereas overexpression of C/ EBPb LIP alone markedly suppressed miR-203. In addition, we demonstrated that C/EBPb LIP inhibited miR-203 transcription by directly interacting with a conserved distal regulatory element upstream of the miR-203 locus, and in doing so, orchestrated chromatin remodeling. In conclusion, our results have revealed a new regulatory mechanism that involves C/EBPb-LIP-mediated downregulation of miR-203, which plays a key role in EMT and metastasis.

show abstract

“…CCAAT/enhancer binding protein β (C/EBPβ) plays an important role in GBM cell growth, migration and invasion through EMT regulation, reduction of its expression inhibits the growth and invasion of glioblastoma cells343738. In epithelial to mesenchymal transition, E-cadherin is a marker of epithelial phenotype, while, N-cadherin and vimentin are the markers for mesenchymal phenotype39; Twist, slug and snail are the master regulators of the epithelial-mesenchymal transition4041, they worked coordinately in regulation of GBM cell migration, invasion and metastasis through induction of EMT.…”

Section: Discussionmentioning

confidence: 99%

Kukoamine A inhibits human glioblastoma cell growth and migration through apoptosis induction and epithelial-mesenchymal transition attenuation

Wang

Sun

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Cortex lycii radicis is the dried root bark of Lycium chinense, a traditional Chinese herb used in multiple ailments. The crude extract of Cortex lycii radicis has growth inhibition effect on GBM cells. Kukoamine A (KuA) is a spermine alkaloid derived from it. KuA possesses antioxidant, anti-inflammatory activities, but its anticancer activity is unknown. In this study, the growth and migration inhibition effect of KuA on human GBM cells and the possible mechanism of its activity were investigated. After KuA treatment, proliferation and colony formation of GBM cells were decreased significantly; apoptotic cells were increased; the cell cycle was arrested G0/G1 phase; the migration and invasion were decreased, the growth of tumors initiated from GBM cells was inhibited significantly; the expressions of 5-Lipoxygenase (5-LOX) were decreased, apoptotic proteins, Bax and caspase-3 were increased, and antiapoptotic protein Bcl-2 was decreased significantly; The expressions of CCAAT/enhancer binding protein β (C/EBPβ), N-cadherin, vimentin, twist and snail+slug were decreased significantly, while the expression of E-cadherin was increased significantly in KuA treated GBM cells and tumor tissues. KuA inhibited human glioblastoma cell growth and migration in vitro and in vivo through apoptosis induction and epithelial-mesenchymal transition attenuation by downregulating expressions of 5-LOX and C/EBPβ.

show abstract

Increased expression of CCAAT/enhancer binding protein β correlates with prognosis in glioma patients

Cited by 28 publications

References 32 publications

Glial Progenitors as Targets for Transformation in Glioma

Glial Progenitors as Targets for Transformation in Glioma

Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Kukoamine A inhibits human glioblastoma cell growth and migration through apoptosis induction and epithelial-mesenchymal transition attenuation

Contact Info

Product

Resources

About