Correlation of glucocorticoid-mediated E4BP4 upregulation with altered expression of pro- and anti-apoptotic genes in CEM human lymphoblastic leukemia cells

Beach, Jessica A.; Nary, Laura J; Hovanessian, Rebeka; Medh, Rheem D.

doi:10.1016/j.bbrc.2014.07.103

Cited by 6 publications

(3 citation statements)

References 28 publications

(39 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The up-regulated genes include Fas, TNF-α related genes, caspases and pro-apoptotic Bcl-2 family members. The down-regulated genes include Card 10, II10 and Birc3, which are mainly anti-apoptotic [17]. …”

Section: Resultsmentioning

confidence: 99%

Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells

Wang

Parrish

2015

Apoptosis

View full text Add to dashboard Cite

The aging kidney undergoes structural and functional alterations which make it more susceptible to drug-induced acute kidney injury (AKI). Previous studies in our lab have shown that the expression of α(E)-catenin is decreased in aged kidney and loss of α(E)-catenin potentiates AKI-induced apoptosis, but not necrosis, in renal tubular epithelial cells (NRK-52E cells). However, the specific apoptotic pathway underlying the increased AKI-induced cell death is not yet understood. In this study, cells were challenged with nephrotoxicant cisplatin to induce AKI. A ~5.5-fold increase in Fas expression in C2 (stable α(E)-catenin knockdown) relative to NT3 (non-targeted control) cells was seen. Increased caspase-8 and -9 activation was induced by cisplatin in C2 as compared to NT3 cells. In addition, decreased Bcl-2 expression and increased BID cleavage and cytochrome C release were detected in C2 cells after cisplatin challenge. Treating the cells with cisplatin, in combination with a Bcl-2 inhibitor, decreased the viability of NT3 cells to the same level as C2 cells after cisplatin. Furthermore, caspase-3/-7 activation is blocked by Fas, caspase-8, caspase-9 and pan-caspase inhibitors. These inhibitors also completely abolished the difference in viability between NT3 and C2 cells in response to cisplatin. These results demonstrate a Fas-mediated apoptotic signaling pathway that is enhanced by the age-dependent loss of α(E)-catenin in renal tubule epithelial cells.

show abstract

Section: Resultsmentioning

confidence: 99%

Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells

Wang

Parrish

2015

Apoptosis

View full text Add to dashboard Cite

show abstract

“…Treatment with DIM significantly reduced the expression of a transcript associated with human apoptosis (TRAF4) ( 86 ). Glucocorticoid-mediated E4BP4 promotes apoptotic effects in CEM lymphocytic leukaemia cells through upregulation, whereas TRAF4 expression in contrast to E4BP4 inhibits apoptosis in lymphocytic leukaemia cells ( 87 ) ( Table 2 ).…”

Section: Regulatory Role In Other Tumorsmentioning

confidence: 99%

The Research Progress in Physiological and Pathological Functions of TRAF4

Ruan

Zhang

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

Tumour necrosis factor receptor-associated factor 4 (TRAF4) is a member of the TRAF protein family, a cytoplasmic bridging molecule closely associated with various immune functions. The physiological processes of TRAF4 are mainly involved in embryonic development, cell polarity, cell proliferation, apoptosis, regulation of reactive oxygen species production. TRAF4 is overexpressed in a variety of tumors and regulates the formation and development of a variety of tumors. In this review, we summarize the physiological and pathological regulatory functions of TRAF4 and focus on understanding the biological processes involved in this gene, to provide a reference for further studies on the role of this gene in tumorigenesis and development.

show abstract

“…The primary action of GCs is mediated through their interactions with the GR, a transcription factor from the nuclear receptor family, which modulates up or down regulation of genes containing GC Responsive Elements (GRE) or through interactions with other transcription factors, coactivators and corepressors [2]. We [4, 5] and others [6, 7] have analyzed changes in gene expression profiles induced by GCs in an effort to identify candidate genes modulating GC-evoked apoptosis of leukemic lymphoid cells. We have identified a panel of genes, including RCAN1 , E4BP4 and Bcl2L11 ( BIM ) as significantly upregulated in CEM-C7-14 cells which are susceptible to GC-evoked apoptosis, but not in CEM-C1-15 cells, which are refractory to GC-evoked apoptosis [4, 5, 8, 9].…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid-mediated co-regulation of RCAN1-1, E4BP4 and BIM in human leukemia cells susceptible to apoptosis

Saenz

Hovanessian

Gisis

et al. 2015

Biochemical and Biophysical Research Communications

Self Cite

View full text Add to dashboard Cite

Glucocorticoids (GCs) are known to induce apoptosis of leukemia cells via gene regulatory changes affecting key pro-and anti-apoptotic genes. Three genes previously implicated in GC-evoked apoptosis in the CEM human T-cell leukemia model, RCAN1, E4BP4 and BIM, were studied in a panel of human lymphoid and myeloid leukemia cell lines. Of the two RCAN1 transcripts, the synthetic GC Dexamethasone (Dex) selectively upregulates RCAN1-1, but not RCAN1-4, in GC-susceptible Sup-B15, RS4;11, Kasumi-1 cells but not in GC-resistant Sup T1 and Loucy cells. E4BP4 and BIM regulation correlated with that of RCAN1-1. A putative GRE and four EBPREs were identified within 1500bp upstream from the transcription start site of RCAN1-1. GC-refractory CEM C1-15 cells sensitized to GC-evoked apoptosis by ectopic E4BP4 expression, CEM C1-15mE#3, showed restored RCAN1-1 upregulation, suggesting that RCAN1-1 is a downstream target of E4BP4. A model for coordinated regulation of RCAN1-1, E4BP4 and BIM, and their role in GC-evoked apoptosis is proposed.

show abstract

Correlation of glucocorticoid-mediated E4BP4 upregulation with altered expression of pro- and anti-apoptotic genes in CEM human lymphoblastic leukemia cells

Cited by 6 publications

References 28 publications

Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells

Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells

The Research Progress in Physiological and Pathological Functions of TRAF4

Glucocorticoid-mediated co-regulation of RCAN1-1, E4BP4 and BIM in human leukemia cells susceptible to apoptosis

Contact Info

Product

Resources

About