Tumor growth inhibition of metastatic nasopharyngeal carcinoma cell lines by low dose of arsenic trioxide via alteration of cell cycle progression and induction of apoptosis

Yeh, Kun‐Yun; Chang, Jeng-Shou; Li, Yingying; Wang, Cheng‐Hsu; Wang, Hung‐Ming

doi:10.1002/hed.21535

Cited by 7 publications

(6 citation statements)

References 43 publications

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“…LRIG1-siRNA cells exhibited higher proliferative ability compared with the negative control cells. Consistent with a previous report that cell cycle progression was involved in the process of tumor growth (24), our study revealed a profound effect of LRIG1-knockdown on cell cycle distribution, evidenced by an accumulation of cells in the G2/M phase. G2/M-arrested cells were observed to express an increased amount of survivin to resist chemotherapy (25), indicating that the downregulation of LRIG1 in glioblastoma cells may enhance the capability of chemotherapy resistance.…”

Section: Discussionsupporting

confidence: 92%

Downregulation of LRIG1 expression by RNA interference promotes the aggressive properties of glioma cells via EGFR/Akt/c-Myc activation

et al. 2012

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The LRIG1 [leucine-rich repeats and immunoglobulin-like domains (LRIG)] gene is not universally downregulated in human cancers, and its role in tumorigenesis and the development of glioma has not been well addressed. In this study, we used short hairpin RNA (shRNA)-triggered RNA interference (RNAi) to block LRIG1 gene expression in the GL15 human glioma cell line. Specific downregulation of LRIG1 by shRNA resulted in significantly enhanced capabilities of proliferation, inhibition of apoptosis and invasion in the GL15 cells. LRIG1 repression induced marked activation of epidermal growth factor receptor (EGFR), protein kinase B (Akt) and c-Myc signaling molecules. Our results demonstrated that RNAi against LRIG1 may effectively downregulate LRIG1 gene expression. LRIG1 functions as a tumor suppressor in the pathogenesis of glioma via EGFR/Akt/c-Myc activation.

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Section: Discussionsupporting

confidence: 92%

Downregulation of LRIG1 expression by RNA interference promotes the aggressive properties of glioma cells via EGFR/Akt/c-Myc activation

et al. 2012

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“…” In contrast, various forms of arsenic have also been used for centuries to treat a wide range of illnesses, including syphilis, malaria, asthma, chorea, eczema, psoriasis, and cancer [23]. Today, one molecular species of arsenic, arsenic trioxide (As 2 O 3 ) is an FDA-approved therapy to treat acute promyelocytic leukemia and also shows promising anticancer activity in laboratory models of other human cancers [24–26]. In the most common setting, however, that of chronic low dose, environmental exposures, arsenicals are associated with a number of human maladies, among them cancer, neurologic disorders, cardiovascular disease, developmental abnormalities, and diabetes [27–30].…”

Section: 4 Epigenetic Remodeling By Environmental Arsenicalsmentioning

confidence: 99%

Epigenetic Changes During Cell Transformation

Futscher

2012

Advances in Experimental Medicine and Biology

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Malignant cancer emerges from normal healthy cells in a multistep process that involves both genetic and epigenetic lesions. Both genetic and environmental inputs participate in driving the epigenetic changes that occur during human carcinogenesis. The pathologic changes seen in DNA methylation and histone posttranslational modifications are complex, deeply intertwined, and act in concert to produce malignant transformation. To better understand the causes and consequences of the pathoepigenetic changes in cancer formation, a variety of experimentally tractable human cell line model systems that accurately reflect the molecular alterations seen in the clinical disease have been developed. Results from studies using these cell line model systems suggest that early critical epigenetic events occur in a stepwise fashion prior to cell immortalization. These epigenetic steps coincide with the cell's transition through well-defined cell proliferation barriers of stasis and telomere dysfunction. Following cell immortalization, stressors, such as environmental toxicants, can induce malignant transformation in a process in which the epigenetic changes occur in a smoother progressive fashion, in contrast to the stark stepwise epigenetic changes seen prior to cell immortalization. It is hoped that developing a clearer understanding of the identity, timing, and consequences of these epigenetic lesions will prove useful in future clinical applications that range from early disease detection to therapeutic intervention in malignant cancer.

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“…ATO has been utilized alone and in conjunction with radiotherapy in both in vitro and in vivo models of NPC [28-30,32-35]. In studies utilizing tumor xenograft models of NPC, treatment with ATO alone produced a decrease in tumor growth compared to controls at doses of 5–10 mg/kg/d.…”

Section: Discussionmentioning

confidence: 99%

Co-treatment with arsenic trioxide and ganciclovir reduces tumor volume in a murine xenograft model of nasopharyngeal carcinoma

Sides¹,

Sosulski²,

Luo³

et al. 2013

Virol J

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We have previously shown that disruption of promyelocytic leukemia nuclear bodies (PML NBs) is sufficient to activate the EBV lytic cycle thus making infected cells susceptible to ganciclovir (GCV) mediated killing in vitro. Here we show that co-administration of GCV and arsenic trioxide (ATO), a PML NB disruptor, reduces tumor volume in a xenograft model of nasopharyngeal carcinoma utilizing CNE1 cells. When administered at pharmacologic levels, both GCV and ATO reduced tumor growth while co-treatment with GCV + ATO resulted in a diminution of tumor volume. Treatment with GCV or ATO individually resulted in an increased number of apoptotic cells while co-treatment with GCV + ATO synergistically induced apoptosis. Treatment with ATO or co-treatment with GCV + ATO resulted in expression of EBV lytic proteins. These data suggest that co-treatment with GCV + ATO may provide an effective treatment for nasopharyngeal carcinoma patients.

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Tumor growth inhibition of metastatic nasopharyngeal carcinoma cell lines by low dose of arsenic trioxide via alteration of cell cycle progression and induction of apoptosis

Abstract: ATO at low dose seems to be an encouraging schedule for palliative treatment of metastatic NPC.

Cited by 7 publications

References 43 publications

Downregulation of LRIG1 expression by RNA interference promotes the aggressive properties of glioma cells via EGFR/Akt/c-Myc activation

Downregulation of LRIG1 expression by RNA interference promotes the aggressive properties of glioma cells via EGFR/Akt/c-Myc activation

Epigenetic Changes During Cell Transformation

Co-treatment with arsenic trioxide and ganciclovir reduces tumor volume in a murine xenograft model of nasopharyngeal carcinoma

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