N-(4-Hydroxyphenyl)retinamide induced differentiation with repression of telomerase and cell cycle to increase interferon-γ sensitivity for apoptosis in human glioblastoma cells

Janardhanan, Rajiv; Banik, Naren L.; Ray, Swapan K.

doi:10.1016/j.canlet.2007.11.016

Cited by 23 publications

(10 citation statements)

References 46 publications

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“…2). It is known that IFNγ induces caspases 3, 8 and 9 in certain cell lines, including glioblastoma and conjunctival epithelial cells (26,27). In the present study, we demonstrated that IFNγ induced these caspases in HCC cells, and that their activation was enhanced by β-catenin overexpression.…”

Section: Discussionsupporting

confidence: 67%

High levels of β-catenin promote IFNγ-induced apoptosis in hepatocellular carcinoma cells

Tong

Huang

et al. 2012

Oncology Letters

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Abstract. β-catenin is a multifunctional protein that is involved in cellular structure and the Wnt/β-catenin signaling pathway. Wnt/β-catenin signaling is believed to be an inducer of cell proliferation in different tumors. However, in certain physiological contexts β-catenin also promotes apoptosis. High levels of β-catenin are found in a number of cancer cell types. Recent studies have shown that β-catenin may be correlated with carcinogenesis. Its effects and interaction with interferon (IFN)γ signaling in hepatocellular carcinoma (HCC) cells remains unknown. In the present study, high levels of β-catenin did not induce antiproliferative effects or apoptosis and did not lead to changes in the levels of caspases or activated STATs. However, high levels of β-catenin did cause positive p53 accumulation and Bcl-XL downregulation in HepG2 cells, a HCC cell line. When treated with IFNγ, apoptosis was induced more rapidly compared with cells with low β-catenin levels (P<0.05), whereas caspases 3, 8 and 9 were markedly activated. The caspase inhibitor Z-VAD-FMK and the STAT3 inhibitor blocked this IFNγ-induced apoptosis. Therefore, we report that high levels of β-catenin promote IFNγ-induced apoptosis in HCC in a caspase-and STAT3-dependent manner, and facilitate the activation of executor caspases, possibly via regulation of p53 and Bcl-XL levels. These findings may provide foundations for the development of new IFN-based therapies against liver cancer.

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Section: Discussionsupporting

confidence: 67%

High levels of β-catenin promote IFNγ-induced apoptosis in hepatocellular carcinoma cells

Tong

Huang

et al. 2012

Oncology Letters

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“…The cells were then washed twice with PBS, pH 7.4 before being fixed in 95% ethanol. The cells were allowed to dry before Wright staining [21]. Finally, the morphological features of the cells (n=300) were observed under the light microscope, as we described recently [21].…”

Section: Methodsmentioning

confidence: 99%

N-Myc down regulation induced differentiation, early cell cycle exit, and apoptosis in human malignant neuroblastoma cells having wild type or mutant p53

Janardhanan

Banik

Ray

2009

Biochemical Pharmacology

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Neuroblastomas, which mostly occur in children, are aggressive metastatic tumors of the sympathetic nervous system. The failure of the previous therapeutic regimens to target multiple components of N-Myc pathway resulted in poor prognosis. The present study investigated the efficacy of the combination of N-(4-hydroxyphenyl) retinamide (4-HPR, 0.5 μM) and genistein (GST, 25 μM) to control the growth of human neuroblastoma cells (SH-SY5Y and SK-N-BE2) harboring divergent molecular attributes. Combination of 4-HPR and GST down regulated NMyc, Notch-1, and Id2 to induce neuronal differentiation. Transition to neuronal phenotype was accompanied by increase in expression of e-cadherin. Induction of neuronal differentiation was associated with decreased expression of hTERT, PCNA, survivin, and fibronectin. This is the first report that combination of 4-HPR and GST mediated reactivation of multiple tumor suppressors (p53, p21, Rb, and PTEN) for early cell cycle exit (due to G1/S phase arrest) in neuroblastoma cells. Reactivation of tumor suppressor(s) repressed N-Myc driven growth factor mediated angiogenic and invasive pathways (VEGF, b-FGF, MMP-2, and MMP-9) in neuroblastoma. Repression of angiogenic factors led to the blockade of components of mitogenic pathways [phospho-Akt (Thr 308), p65 NF-κB and p42/44 Erk 1/2]. Taken together, the combination of 4-HPR and GST effectively blocked survival, mitogenic, and angiogenic pathways and activated proteases for apoptosis in neuroblastoma cells. These results suggested that combination of 4-HPR and GST could be effective for controlling the growth of heterogeneous human neuroblastoma cell populations.

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“…The cells were then washed twice with PBS, pH 7.4, before Wright staining. The 6-well plates were then allowed to dry and examined under the light microscope, as we reported previously (Janardhanan et al, 2008). The morphological features of apoptotic cells included at least one of such characteristics as cell shrinkage, chromatin condensation, and membrane-bound apoptotic bodies.…”

Section: Methodsmentioning

confidence: 99%

Alterations in expression of specific microRNAs by combination of 4-HPR and EGCG inhibited growth of human malignant neuroblastoma cells

et al. 2012

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Malignant neuroblastomas are childhood tumors that remain mostly incurable. We explored efficacy of N-(4-hydroxyphenyl) retinamide (4-HPR) and (−)-epigallocatechin-3-gallate (EGCG) in altering expression of oncogenic microRNAs (OGmiRs) and tumor suppressor miRs (TSmiRs) for controlling growth of human malignant neuroblastoma SK-N-BE2 and IMR-32 cells. Combination of 4-HPR and EGCG most significantly decreased expression of OGmiRs (miR-92, miR-93, and miR-106b) and increased expression of TSmiRs (miR-7-1, miR-34a, and miR-99a) in both cell lines. Overexpression of miR-93 and miR-7-1, respectively, decreased and increased efficacy of treatments. Thus, alterations in expression of specific OGmiRs and TSmiRs by 4-HPR and EGCG inhibited growth of malignant neuroblastomas.

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N-(4-Hydroxyphenyl)retinamide induced differentiation with repression of telomerase and cell cycle to increase interferon-γ sensitivity for apoptosis in human glioblastoma cells

Cited by 23 publications

References 46 publications

High levels of β-catenin promote IFNγ-induced apoptosis in hepatocellular carcinoma cells

High levels of β-catenin promote IFNγ-induced apoptosis in hepatocellular carcinoma cells

N-Myc down regulation induced differentiation, early cell cycle exit, and apoptosis in human malignant neuroblastoma cells having wild type or mutant p53

Alterations in expression of specific microRNAs by combination of 4-HPR and EGCG inhibited growth of human malignant neuroblastoma cells

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