TARBP2是一種RNA 結合蛋白，作為與Dicer 結合的輔因子參與 miRNA 加工。已知TARBP2的表達及其對不同癌細胞系的影響各不相同。與正常乳腺組織相比，乳腺癌中TARBP2的表達水平顯著更高。此外，轉移性乳腺癌有著更高的 TARBP2表現量。在先前的研究中，TARBP2表達水平在他莫昔芬抗藥性細胞株中堆積以促進Merlin-TARBP2通路上調SOX2。這些文獻指出TARBP2參與多面向的促癌功能，但目前並無針對TARBP2在乳腺癌中進行系統性分析以探討其調節的信號通路。在這項研究中，我們利用生物資訊學分析發現了TARBP2過表達的乳腺癌細胞中可能活化的訊息路徑。我們的實驗不但證實TARBP對訊息路徑的活化也進一步找出可能調控的目標基因。總結來說，本研究為一個鑑定出乳癌中TARBP2調控機制以及參與分子的先導成果。

TARBP2 was a RNA-binding protein that participates in miRNA processing as a cofactor binding to Dicer. The expression of TARBP2 varied as well as its effects on different cancer cell types. In breast cancer, TARBP2 level is significantly higher in cancer tissues comparing to normal counterparts. In addition, metastatic breast cancers expresses elevated TARBP2. In our previous study, the TARBP2 expression level was accumulated in tamoxifen-resistant breast cancer cells to upregulate SOX2 through Merlin-TARBP2 pathway. These evidences implies the multifaceted oncogenic functions regulated by TARBP2, but there is no systematic analysis to uncover TARBP2-regulated signaling pathway in breast cancer. In this study, we utilized bioinformatics analyses and found the activation of signaling pathways enriched in gene expression profile of TARBP2-overexpressed breast cancer cells. Our experiments not only showed that TARBP2 expression enhances the activation of signaling pathways in breast cancer cells, but also identified several target genes involved in signaling activation. Our study demonstrated that mechanism of TARBP2-induced AKT pathway was activated. Taken together, this is the pilot study discovered TARBP2-regulated molecular mechanisms and possible regulators in breast cancer.

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