瀰漫性大B細胞淋巴瘤(diffuse large B cell lymphoma, DLBCL)是常見的非霍奇金淋巴瘤(non-Hodgkin lymphoma, NHL)之一，其中類活化B細胞型(activated B cell like, ABC) DLBCL對常規化療具有顯著的抗性。有研究顯示microRNA-155 (miR-155)過度表達與ABC DLBCL腫瘤過度增生以及藥物抗性有關。因此，鎖定miR-155成為一個潛在的治療策略。本研究旨在開發一種結構經過優化的anti-miR-155分子，並利用AS1411適體修飾的陽性脂質體將anti-miR-155精準遞送至ABC DLBCL細胞，以克服miRNA治療的降解和快速清除問題，評估其對腫瘤增殖、化療敏感性及多重耐藥性蛋白表達的調控效果。為提高抗miR-155分子的穩定性與抗降解能力，本研究設計鎖核酸(locked nucleic acid, LNA)修飾及硫代磷酸酯鍵(phosphorothioate, PS)的髮夾(hairpin)結構anti-miR-155 (amiR-H)。本研究亦透過AS1411適體修飾的陽性脂質體，實現anti-miR-155分子的靶向遞送，並在ABC DLBCL細胞株(SU-DHL-2)中評估其治療效果。研究結果顯示，anti-miR-155能顯著提高SU-DHL-2細胞對化療藥物(doxorubicin)處理之化療敏感性。amiR-H通過抑制miR-155上調SMAD5表達，導致SU-DHL-2細胞發生G0/G1期細胞週期停滯，亦顯著上調TP53的表達，促進cytochrome C釋放，增強其介導的細胞凋亡作用。此外，amiR-H通過提升IB的表達並抑制其磷酸化，有效阻斷NF-B轉錄活性。這些作用進一步抑制B細胞分化，並下調多重耐藥性基因ABCG2與ABCB1表達。本研究證實使用amiR-H型修飾的抗miR-155分子結合AS1411修飾脂質體的傳遞系統，可有效抑制ABC DLBCL細胞增生、誘導腫瘤細胞凋亡，能促進化療敏感性，從而抑制腫瘤進展。

Diffuse large B cell lymphoma (DLBCL) is one of the most common types of non-Hodgkin lymphoma (NHL), with the activated B cell-like (ABC) subtype of DLBCL presenting significant resistance to conventional chemotherapy. Previous studies indicated that overexpression of microRNA-155 (miR-155) is associated with tumor proliferation and drug resistance, exacerbating disease progression in ABC DLBCL. Targeting miR-155 has emerged as a potential therapeutic strategy. This study aims to develop an optimized anti-miR-155 molecule and utilize AS1411 aptamer-modified cationic liposomes to precisely deliver anti-miR-155 to ABC DLBCL cells, addressing the challenges of degradation and rapid clearance in miRNA therapy while evaluating its effects on tumor proliferation, chemotherapy sensitivity, and multidrug resistance protein expression. To enhance stability, this study designed a hairpin structure anti-miR-155 (amiR-H) incorporating locked nucleic acid (LNA) modifications and phosphorothioate (PS) linkages. AS1411-modified liposomes also employed for targeted delivery of anti-miR-155, and evaluated its therapeutic efficacy in ABC DLBCL cell line (SU-DHL-2). The results of this study indicated that anti-miR-155 significantly enhanced the cytotoxic effects of doxorubicin treatment in SU-DHL-2 cells. amiR-H upregulated SMAD5 expression by inhibiting miR-155, leading to G0/G1 phase cell cycle arrest in SU-DHL-2 cells, and also significantly increased TP53 expression, promoting cytochrome C release and enhancing apoptosis. Additionally, amiR-H effectively blocked NF-κB transcriptional activity by upregulating IκBα expression and inhibiting its phosphorylation. These effects further suppressed B-cell differentiation and downregulated the expression of multidrug resistance genes ABCG2 and ABCB1. This study confirmed that the delivery system combining amiR-H-modified anti-miR-155 molecules with AS1411-modified liposomes can effectively inhibit cell proliferation and induce tumor cell apoptosis, suggesting enhanced chemotherapy sensitivity and consequent suppression of tumor progression in ABC DLBCL.

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