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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

Therapeutically Silencing of EBV-miR-BART7-3p inhibited tumorigenicity of EBV-positive NPC cells in vivo(A) The in vivo effectiveness of nano-anti-miR was evaluated in xenograft mouse models bearing tumors originating from HONE1-EBV cells. (B) The tumor volume was periodically tested for each mouse and tumor growth curve was plotted. Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The expression of PTEN, p-Akt, c-Myc and CCND1 was analyzed by western blot in the tumor tissues derived from therapeutic and control models respectively. β-actin served as an internal control.
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Figure 5: Therapeutically Silencing of EBV-miR-BART7-3p inhibited tumorigenicity of EBV-positive NPC cells in vivo(A) The in vivo effectiveness of nano-anti-miR was evaluated in xenograft mouse models bearing tumors originating from HONE1-EBV cells. (B) The tumor volume was periodically tested for each mouse and tumor growth curve was plotted. Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The expression of PTEN, p-Akt, c-Myc and CCND1 was analyzed by western blot in the tumor tissues derived from therapeutic and control models respectively. β-actin served as an internal control.

Mentions: We further evaluated the in vivo effectiveness of nano-anti-miR in mice bearing tumors originating from HONE1-EBV cells. The nano-anti-miR was injected into the solid tumor of each mouse per three days according to the results of in vitro experiments. During the 18-day treatment, tumor volume was periodically tested and growth curve was plotted. Consistently, we observed that nano-anti-miR obviously inhibited tumor growth compared with NC control or nano-carrier groups (Figure 5A and 5B). Western blot assay confirmed that PTEN expression was also decreased in tumor tissues, whereas p-Akt, c-Myc and CCND1 were increased after the treatment of nano-anti (Figure 5C).


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)

Therapeutically Silencing of EBV-miR-BART7-3p inhibited tumorigenicity of EBV-positive NPC cells in vivo(A) The in vivo effectiveness of nano-anti-miR was evaluated in xenograft mouse models bearing tumors originating from HONE1-EBV cells. (B) The tumor volume was periodically tested for each mouse and tumor growth curve was plotted. Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The expression of PTEN, p-Akt, c-Myc and CCND1 was analyzed by western blot in the tumor tissues derived from therapeutic and control models respectively. β-actin served as an internal control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Therapeutically Silencing of EBV-miR-BART7-3p inhibited tumorigenicity of EBV-positive NPC cells in vivo(A) The in vivo effectiveness of nano-anti-miR was evaluated in xenograft mouse models bearing tumors originating from HONE1-EBV cells. (B) The tumor volume was periodically tested for each mouse and tumor growth curve was plotted. Data were shown as the mean ± SEM (**P < 0.01, ***P < 0.001). (C) The expression of PTEN, p-Akt, c-Myc and CCND1 was analyzed by western blot in the tumor tissues derived from therapeutic and control models respectively. β-actin served as an internal control.
Mentions: We further evaluated the in vivo effectiveness of nano-anti-miR in mice bearing tumors originating from HONE1-EBV cells. The nano-anti-miR was injected into the solid tumor of each mouse per three days according to the results of in vitro experiments. During the 18-day treatment, tumor volume was periodically tested and growth curve was plotted. Consistently, we observed that nano-anti-miR obviously inhibited tumor growth compared with NC control or nano-carrier groups (Figure 5A and 5B). Western blot assay confirmed that PTEN expression was also decreased in tumor tissues, whereas p-Akt, c-Myc and CCND1 were increased after the treatment of nano-anti (Figure 5C).

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