Abstract：
A limited number of studies are devoted to regulating TRIP6 expression in cancer. Hence, we aimed to unveil the regulation of TRIP6 expression in MCF-7 breast cancer cells (with high TRIP6 expression) and taxane-resistant MCF-7 sublines (manifesting even higher TRIP6 expression). We found that TRIP6 transcription is regulated primarily by the cyclic AMP response element (CRE) in hypomethylated proximal promoters in both taxane-sensitive and taxane-resistant MCF-7 cells. Furthermore, in taxane-resistant MCF-7 sublines, TRIP6 co-amplification with the neighboring ABCB1 gene, as witnessed by fluorescence in situ hybridization (FISH), led to TRIP6 overexpression. Ultimately, we found high TRIP6 mRNA levels in progesterone receptor-positive breast cancer and samples resected from premenopausal women.
摘要：
有限数量的研究致力于调节癌症中的TRIP6表达。因此，我们旨在揭示MCF-7乳腺癌细胞(TRIP6高表达)和紫杉烷抗性MCF-7亚系(显示更高的TRIP6表达)中TRIP6表达的调节.我们发现，在紫杉烷敏感和紫杉烷抗性MCF-7细胞中，TRIP6转录主要受低甲基化近端启动子中的环AMP反应元件（CRE）调节。此外，在紫杉烷抗性MCF-7亚系中，TRIP6与邻近的ABCB1基因共扩增，如荧光原位杂交(FISH)所示，导致TRIP6过表达。最终,我们在孕激素受体阳性乳腺癌和绝经前女性切除的样本中发现了较高的TRIP6mRNA水平.
