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Gold nano-particles (AuNPs) carrying anti-EBV-miR-BART7-3p inhibit growth of EBV-positive nasopharyngeal carcinoma.

Cai L, Li J, Zhang X, Lu Y, Wang J, Lyu X, Chen Y, Liu J, Cai H, Wang Y, Li X - Oncotarget (2015)

Bottom Line: Based on these results, we conducted a therapeutic experiment by using gold nano-particles (AuNPs) carrying anti-EBV-miR-BART7-3p.Silencing of EBV-miR-BART7-3p reduced tumor growth in animal model.We conclude that EBV-miR-BART7-3p favors carcinogenesis, representing a potential target for miRNA-based therapy.

View Article: PubMed Central - PubMed

Affiliation: Cancer Research Institute, Southern Medical University, Guangzhou 510515, China.

ABSTRACT
Epstein-Barr virus (EBV) infection is a major etiological factor for nasopharyngeal carcinoma (NPC). Several EBV-encoded BART miRNAs have been associated with viral latency, immune escape, cell survival, cell proliferation and apoptosis. Here, we report that EBV-miR-BART7-3p, an EBV-encoded BART miRNA highly expressed in NPC, was correlated with cell-cycle progression in vitro and increased tumor formation in vivo. This viral miRNA stimulated the PTEN/PI3K/Akt pathway and induced c-Myc and c-Jun. Knockdown of PTEN mimicked EBV-miR-BART7-3p-induced tumorigenic phenotype. Based on these results, we conducted a therapeutic experiment by using gold nano-particles (AuNPs) carrying anti-EBV-miR-BART7-3p. Silencing of EBV-miR-BART7-3p reduced tumor growth in animal model. We conclude that EBV-miR-BART7-3p favors carcinogenesis, representing a potential target for miRNA-based therapy.

No MeSH data available.


Related in: MedlinePlus

Knockdown of PTEN mimicked the EBV-miR-BART7-3p-induced phenotype in NPC cells(A, B) Cell growth and proliferation ability was detected by MTT assay and in colony formation assay in CNE1 and 5-8F cells following the treatment of siRNA against PTEN (si-PTEN for short) or si-NC (Control). Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The cell-cycle transition from G1 to S and G2 was evaluated by the flow cytometry after PTEN was silenced in vitro. Data were shown as the mean ± SEM (*P < 0.05, **P < 0.01). (D) The expression levels of PTEN, p-Akt, c-Myc, CCND1 and CCNE1 were analyzed by western blot in indicated cells after treated with si-PTEN. β-actin is internal control.
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Figure 3: Knockdown of PTEN mimicked the EBV-miR-BART7-3p-induced phenotype in NPC cells(A, B) Cell growth and proliferation ability was detected by MTT assay and in colony formation assay in CNE1 and 5-8F cells following the treatment of siRNA against PTEN (si-PTEN for short) or si-NC (Control). Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The cell-cycle transition from G1 to S and G2 was evaluated by the flow cytometry after PTEN was silenced in vitro. Data were shown as the mean ± SEM (*P < 0.05, **P < 0.01). (D) The expression levels of PTEN, p-Akt, c-Myc, CCND1 and CCNE1 were analyzed by western blot in indicated cells after treated with si-PTEN. β-actin is internal control.

Mentions: The siRNA against PTEN (si-PTEN) was also transfected into CNE1 and 5-8F cells. As expected, si-PTEN-transfected CNE1 and 5-8F-cells presented a higher ability to grow and proliferate relative to the control cells (Figure 3A and 3B). Similarly, flow cytometry analysis revealed an increased percentage of G2 phase cells in two NPC cell lines after introducing si-PTEN (Figure 3C). Western blotting assay confirmed a reduced PTEN protein expression in both CNE1 and 5-8F cells after 72 h transfection of si-PTEN (Figure 3D), followed by an obviously induced expression of p-Akt, c-Myc, c-Jun, CCND1 and CCNE1 (Figure 3D). These results supported that knockdown of PTEN mimicked the EBV-miR-BART7-3p-induced tumorigenic phenotype.


Gold nano-particles (AuNPs) carrying anti-EBV-miR-BART7-3p inhibit growth of EBV-positive nasopharyngeal carcinoma.

Cai L, Li J, Zhang X, Lu Y, Wang J, Lyu X, Chen Y, Liu J, Cai H, Wang Y, Li X - Oncotarget (2015)

Knockdown of PTEN mimicked the EBV-miR-BART7-3p-induced phenotype in NPC cells(A, B) Cell growth and proliferation ability was detected by MTT assay and in colony formation assay in CNE1 and 5-8F cells following the treatment of siRNA against PTEN (si-PTEN for short) or si-NC (Control). Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The cell-cycle transition from G1 to S and G2 was evaluated by the flow cytometry after PTEN was silenced in vitro. Data were shown as the mean ± SEM (*P < 0.05, **P < 0.01). (D) The expression levels of PTEN, p-Akt, c-Myc, CCND1 and CCNE1 were analyzed by western blot in indicated cells after treated with si-PTEN. β-actin is internal control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4480720&req=5

Figure 3: Knockdown of PTEN mimicked the EBV-miR-BART7-3p-induced phenotype in NPC cells(A, B) Cell growth and proliferation ability was detected by MTT assay and in colony formation assay in CNE1 and 5-8F cells following the treatment of siRNA against PTEN (si-PTEN for short) or si-NC (Control). Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The cell-cycle transition from G1 to S and G2 was evaluated by the flow cytometry after PTEN was silenced in vitro. Data were shown as the mean ± SEM (*P < 0.05, **P < 0.01). (D) The expression levels of PTEN, p-Akt, c-Myc, CCND1 and CCNE1 were analyzed by western blot in indicated cells after treated with si-PTEN. β-actin is internal control.
Mentions: The siRNA against PTEN (si-PTEN) was also transfected into CNE1 and 5-8F cells. As expected, si-PTEN-transfected CNE1 and 5-8F-cells presented a higher ability to grow and proliferate relative to the control cells (Figure 3A and 3B). Similarly, flow cytometry analysis revealed an increased percentage of G2 phase cells in two NPC cell lines after introducing si-PTEN (Figure 3C). Western blotting assay confirmed a reduced PTEN protein expression in both CNE1 and 5-8F cells after 72 h transfection of si-PTEN (Figure 3D), followed by an obviously induced expression of p-Akt, c-Myc, c-Jun, CCND1 and CCNE1 (Figure 3D). These results supported that knockdown of PTEN mimicked the EBV-miR-BART7-3p-induced tumorigenic phenotype.

Bottom Line: Based on these results, we conducted a therapeutic experiment by using gold nano-particles (AuNPs) carrying anti-EBV-miR-BART7-3p.Silencing of EBV-miR-BART7-3p reduced tumor growth in animal model.We conclude that EBV-miR-BART7-3p favors carcinogenesis, representing a potential target for miRNA-based therapy.

View Article: PubMed Central - PubMed

Affiliation: Cancer Research Institute, Southern Medical University, Guangzhou 510515, China.

ABSTRACT
Epstein-Barr virus (EBV) infection is a major etiological factor for nasopharyngeal carcinoma (NPC). Several EBV-encoded BART miRNAs have been associated with viral latency, immune escape, cell survival, cell proliferation and apoptosis. Here, we report that EBV-miR-BART7-3p, an EBV-encoded BART miRNA highly expressed in NPC, was correlated with cell-cycle progression in vitro and increased tumor formation in vivo. This viral miRNA stimulated the PTEN/PI3K/Akt pathway and induced c-Myc and c-Jun. Knockdown of PTEN mimicked EBV-miR-BART7-3p-induced tumorigenic phenotype. Based on these results, we conducted a therapeutic experiment by using gold nano-particles (AuNPs) carrying anti-EBV-miR-BART7-3p. Silencing of EBV-miR-BART7-3p reduced tumor growth in animal model. We conclude that EBV-miR-BART7-3p favors carcinogenesis, representing a potential target for miRNA-based therapy.

No MeSH data available.


Related in: MedlinePlus