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<p>Epstein–Barr virus is a double‑stranded DNA virus that plays a key role throughout the development of Burkitt lymphoma. The EBV genome encodes 44 mature microRNAs (miR‑BARTs) that collectively promote tumorigenesis. TP53, a tumor suppressor protein, prevents cancer progess by inducing cell-cycle arrest, apoptosis, and modulating glycolysis. In this study, we found that miR‑BART5‑3p is highly expressed in EBV positive cells and contributes to glycolysis process. Forced expression of miR‑BART5‑3p enhanced the proliferative and migratory capacities, while downregulation of miR‑BART5‑3p led to a reduction in these capacities in Ramos and CA46. Subsequently, we demonstrated that TP53 suppressed the proliferation and migration of Burkitt lymphoma cells. Furthermore, we predicted that EBV-miR‑BART5‑3p targeted 3’‑UTR of TP53 mRNA via RNAhybrid program and the QPCR results indicated that there was a significant converse expression between EBV-miR‑BART5‑3p and TP53 in Raji cells. These results implied that EBV-miR‑BART5‑3p promoted the proliferation of Ramos and CA46 via targeting the 3’‑UTR of TP53 mRNA. Altogether, these findings define a novel mechanism for EBV-miR-BART5-3p through the glycolysis pathway in Burkitt lymphoma development.</p>

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EBV-miR-BART5-3p promotes the proliferation of Burkitt lymphoma cells via glycolytic pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月27日

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  • Dezhuan Da,
  • Yujiao Qi,
  • Chunyan Dang,
  • Li Xue,
  • Xiaomin Huang,
  • Xia Wang,
  • Hongling Li

摘要

Epstein–Barr virus is a double‑stranded DNA virus that plays a key role throughout the development of Burkitt lymphoma. The EBV genome encodes 44 mature microRNAs (miR‑BARTs) that collectively promote tumorigenesis. TP53, a tumor suppressor protein, prevents cancer progess by inducing cell-cycle arrest, apoptosis, and modulating glycolysis. In this study, we found that miR‑BART5‑3p is highly expressed in EBV positive cells and contributes to glycolysis process. Forced expression of miR‑BART5‑3p enhanced the proliferative and migratory capacities, while downregulation of miR‑BART5‑3p led to a reduction in these capacities in Ramos and CA46. Subsequently, we demonstrated that TP53 suppressed the proliferation and migration of Burkitt lymphoma cells. Furthermore, we predicted that EBV-miR‑BART5‑3p targeted 3’‑UTR of TP53 mRNA via RNAhybrid program and the QPCR results indicated that there was a significant converse expression between EBV-miR‑BART5‑3p and TP53 in Raji cells. These results implied that EBV-miR‑BART5‑3p promoted the proliferation of Ramos and CA46 via targeting the 3’‑UTR of TP53 mRNA. Altogether, these findings define a novel mechanism for EBV-miR-BART5-3p through the glycolysis pathway in Burkitt lymphoma development.