Bo Han1, Shuguo Wang2, Hongguo Zhao3. 1. Department of Hemotology, Qingdao Hiser Hospital Affiliated to Qingdao University Qingdao 266033, Shandong Province, China. 2. Department of Clinical Laboratory, The Affiliated Qingdao Municipal of Qingdao University Qingdao 266003, Shandong Province, China. 3. Department of Hemotology, The Affiliated Qingdao Municipal of Qingdao University Qingdao 266003, Shandong Province, China.
Abstract
INTRODUCTION: Burkitt's lymphoma (BL) is a rare and highly aggressive B cell non-Hodgkin lymphoma. High toxicity of chemotherapy for BL treatment causes morbidity and mortality. Many miRNAs have been used as biomarkers for early detection or therapy targets for tumors. However, the roles of miR-21 and miR-155 in Burkitt's lymphoma remain unclear. METHODS: We collected 15 blood samples from patients with Burkitt's lymphoma and evaluated the expression of miR-21 and miR-155. Then, we knocked down miR-21 and miR-155 expression in Burkitt's lymphoma cell lines and assessed cell proliferation, cell cycle, and apoptosis. Furthermore, we detected the activation of PI3K/AKT pathway by qPCR and western blot. Finally, we predicted the target genes of miR-21 and miR-155 by publicly available databases. RESULTS: The expression of miR-21 and miR-155 in blood samples from patients with Burkitt's lymphoma were significantly upregulated. Knockdown of miR-21 and miR-155 significantly suppressed cell proliferation, and resulted in S phase arrest and cell apoptosis. The knockdown of miR-21 and miR-155 inhibited the activation of the PI3K/AKT pathway. We found that the target genes of miR-21 and miR-155 were C1RL and TCAP. CONCLUSION: miR-21 and miR-155 promote the progression of Burkitt's lymphoma through PI3K/AKT signaling by targeting C1RL and TCAP. Our findings will provide a novel biomarker and therapeutic strategies for Burkitt's lymphoma. IJCEP
INTRODUCTION:Burkitt's lymphoma (BL) is a rare and highly aggressive B cell non-Hodgkin lymphoma. High toxicity of chemotherapy for BL treatment causes morbidity and mortality. Many miRNAs have been used as biomarkers for early detection or therapy targets for tumors. However, the roles of miR-21 and miR-155 in Burkitt's lymphoma remain unclear. METHODS: We collected 15 blood samples from patients with Burkitt's lymphoma and evaluated the expression of miR-21 and miR-155. Then, we knocked down miR-21 and miR-155 expression in Burkitt's lymphoma cell lines and assessed cell proliferation, cell cycle, and apoptosis. Furthermore, we detected the activation of PI3K/AKT pathway by qPCR and western blot. Finally, we predicted the target genes of miR-21 and miR-155 by publicly available databases. RESULTS: The expression of miR-21 and miR-155 in blood samples from patients with Burkitt's lymphoma were significantly upregulated. Knockdown of miR-21 and miR-155 significantly suppressed cell proliferation, and resulted in S phase arrest and cell apoptosis. The knockdown of miR-21 and miR-155 inhibited the activation of the PI3K/AKT pathway. We found that the target genes of miR-21 and miR-155 were C1RL and TCAP. CONCLUSION:miR-21 and miR-155 promote the progression of Burkitt's lymphoma through PI3K/AKT signaling by targeting C1RL and TCAP. Our findings will provide a novel biomarker and therapeutic strategies for Burkitt's lymphoma. IJCEP
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