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BMC Cancer. 2017 Feb 21;17(1):147. doi: 10.1186/s12885-017-3145-4.

Wogonin as a targeted therapeutic agent for EBV (+) lymphoma cells involved in LMP1/NF-κB/miR-155/PU.1 pathway.

Author information

1
Department of Hematology and Oncology (Key Department of Jiangsu Medicine), Medical School, the Affiliated Zhongda Hospital, Southeast University, Nanjing, 210009, China.
2
Department of Gastroenterology, Medical School, The Second Hospital of Nanjing Affiliated to Southeast University, Nanjing, China.
3
State Key Laboratory of Bioelectronics, School of Biological Science and Medical Engineering, Southeast University, Nanjing, China.
4
State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, Nanjing, China.
5
Department of Hematology and Oncology (Key Department of Jiangsu Medicine), Medical School, the Affiliated Zhongda Hospital, Southeast University, Nanjing, 210009, China. cba8888@hotmail.com.

Abstract

BACKGROUND:

Wogonin is an encouraging choice for clinical use owing to its potent anti-tumor and anti-inflammatory effects with the high safety profile. However, wogonin for targeted therapy of lymphoma was not well addressed. In this study, we focused on its anticancer effect alongside with the underlying mechanisms for targeted therapy in EBV-positive lymphoma. This will facilitate its introduction to clinical use, which is planned in the near future.

METHODS:

Cell proliferation was studied by CCK8. Flow cytometry was used to analyze the apoptosis and the cycle arrest of cells. Further, we also used immunofluorescent staining to detect the morphologic changes of the apoptotic cells. The expression of LMP1/miR-155/p65/pp65/PU.1 was evaluated by quantitative real-time PCR (qRT-PCR) and western blot, while that of NF-κB was analyzed by EMSA. At last, immunohistochemical staining was applied to assess the expression of target proteins and relevant molecules.

RESULTS:

In vitro, wogonin induced the apoptosis of Raji cells by downregulating the expression of NF-κB through LMP1/miR-155/NF-κB/PU.1 pathway, which was in a dose and time-dependent manner. In vivo, wogonin could suppress tumor growth, associated with the downregulation of ki67, p65 and upregulation of PU.1.

CONCLUSIONS:

Wogonin could suppress tumor growth and induce cell apoptosis by inhibiting the expression of NF-κB. Taken these findings, we concluded that wogonin could be a potential targeted therapeutic agent for EBV-positive lymphoma with the expression of LMP1 through the pathway of LMP1/NF-κB/miR-155/PU.1.

KEYWORDS:

Apoptosis; EBV infection; Lymphoma; NF-κB; Wogonin

PMID:
28222771
PMCID:
PMC5320633
DOI:
10.1186/s12885-017-3145-4
[Indexed for MEDLINE]
Free PMC Article

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