通過生物資訊學分析揭示miR-29b在乳癌的預測價值和免疫學作用

Unveiling the Prediction Value and Immunological Role of miR-29b in Breast Cancer via Bioinformatic Analysis

乳癌是全球發病率最高的惡性腫瘤，也是全球腫瘤相關死亡的主要原因之一。腫瘤免疫微環境在癌症進展中起著至關重要的作用。儘管miR-29b在乳癌可作為預後標記，但其在形塑腫瘤免疫微環境的重要性尚未清楚。本研究使用生物資訊學數據源，我們發現高miR-29b與較長總生存時間相關，並且乳癌腫瘤比正常組織表達更高的miR-29b。使用單細胞轉錄組數據庫，我們發現miR-29b主要在介導T細胞細胞毒性的細胞中表達，包括自然殺手T細胞、自然殺手細胞、CD8+初始T細胞和CD4+初始T細胞。使用miRDIP數據庫與Metascape演算法的組合，我們發現miR-29b靶向基因主要介導膠原蛋白的形成。使用TansmiR v2.0數據庫和ENCORI平台，我們鑑識IRF1為驅動人類乳癌miR-29b表達的潛在轉錄因子。總之，高miR-29b可作為乳癌患者良好生存的預測因素。miR-29b主要在介導T細胞細胞毒性的細胞中表達。IRF1作為驅動miR-29b的潛在轉錄因子，產生的途徑主要在於膠原蛋白的形成。這些發現為開發針對miR-29b相關網絡的新診斷/預後生物標誌物和治療方法提供了機會。

Breast cancer (BC) is the leading cause of malignant tumors and a major contributor to tumor-related deaths worldwide. The tumor immune microenvironment (TIME) plays a crucial role in cancer progression. Although miR-29b acts as a prognostic indicator for BC, its relevance for shaping TIME is yet to be studied. In this study, we used bioinformatics to investigate the association between miR-29b expression and overall survival time in BC patients. We found that high miR-29b is associated with longer overall survival time and that BC tumor expresses higher miR-29b than normal tissue. Using single cell transcriptomes database, we revealed that miR-29b primarily expresses in cells that mediate T cell cytotoxicity, including NKT, NK, CD8+ naïve T cell and CD4+ naïve T cells. Using the combination of a miRDIP database with the Metascape algorithm, we showed that miR-29b-targeted genes predominantly mediate collagen formation. Using the TansmiR v2.0 database along with the ENCORI platform, we identified IRF1 as a potential transcription factor that drives the expression of miR-29b in human BC. These findings suggest that high miR-29b can serve as a predictive factor for favorable survival in BC patients and provide insight into the underlying mechanisms involved in collagen formation. These findings have the potential to guide the development of a new diagnostic/prognostic biomarker and therapeutic approach targeting the miR-29-bassociated network.