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首页> 外文期刊>Journal of Thoracic Disease >WNT signaling pathway regulator- FRAT2 affects oncogenesis and prognosis of basal-like breast cancer
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WNT signaling pathway regulator- FRAT2 affects oncogenesis and prognosis of basal-like breast cancer

机译：WNT信号通路调节器 - FRAT2会影响基础乳腺癌的癌症和预后

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Background: Breast cancer is the most common malignant cancer in women worldwide and is one of the leading causes of cancer death. Basal-like breast cancer (BLBC) is an aggressive subtype of breast cancer for which targeted therapy has poor efficacy. Therefore, research into the molecular pathogenesis of BLBC is urgent for developing effective targeted therapeutic treatments. Methods: We collected relevant data from the Cancer Genome Atlas (TCGA), including transcriptome, copy number variation, and survival data. We also gathered 30 pairs clinical samples of cancer tissues and non-cancerous tissues to perform Western Blotting (WB) to reveal the encoded protein expression levels. Besides, we knocked down frequently rearranged in advanced T-cell lymphomas 2 (FRAT2) expression in two representative cell lines (T47D and MDA-MB-231 cells). The cell cycle progression was analyzed, while the apoptosis experiments were also conducted to explore the molecular pathogenesis of FRAT2 in BLBC. Results: The aberrant activation of the WNT pathway and highly expressed FRAT2 were specifically identified across the BLBC genome comparing to other types of tumor. In addition, FRAT2 expression was found to be positively associated with its copy number variations (P=9.126×10?23). For further investigation, we found the expression level of FRAT2 was related to the poor overall survival of BLBC patients (P=0.049). The results of WB revealed that FRTA2-encoded protein was overexpressed in BLBC tissues. Based on results in T47D and MDA-MB-231 cells in vitro, we found that knocking down FRAT2 can inhibit the proliferation of these two cell lines. In cell cycle progression experiments, cell cycle arrested in the G2/M phase. Meanwhile, increased apoptosis was also found in the shFRAT2 cell group in vitro. Conclusions: In BLBC basal-like breast cancer, we can assume that FRAT2 is a potential treatment target.
机译：背景：乳腺癌是全球妇女中最常见的恶性癌症，是癌症死亡的主要原因之一。基础乳腺癌（BLBC）是一种乳腺癌的侵略性亚型，靶向治疗的疗效差。因此，对BLBC的分子发病机制的研究是迫在意用于显影有效的靶向治疗处理。方法：我们从癌症基因组地图集（​​TCGA）收集相关数据，包括转录组，拷贝数变异和生存数据。我们还聚集了30对癌组织和非癌组织的临床样本，以进行蛋白质印迹（WB）以露出编码的蛋白质表达水平。此外，我们在两种代表性细胞系（T47D和MDA-MB-231细胞中，我们经常被击倒在先进的T细胞淋巴瘤2（FRAT2）表达中被重新排列。分析细胞周期进展，同时还进行了细胞凋亡实验以探讨BLBC中FRAT2的分子发病机制。结果：WNT途径的异常活化和高表达的FRAT2在短短的基因组上鉴定到与其他类型的肿瘤相比。此外，发现FRAT2表达与其拷贝数变化正相关（P = 9.126×10？23）。为了进一步调查，我们发现FRAT2的表达水平与BLBC患者的整体存活差有关（P = 0.049）。 WB的结果显示在短文组织中过表达FRTA2编码蛋白。基于T47D和MDA-MB-231细胞在体外的结果，我们发现敲击FRAT2可以抑制这两种细胞系的增殖。在细胞周期进展实验中，细胞周期在G2 / M相中停止。同时，在体外的SHFRAT2细胞基团中也发现了增加的细胞凋亡。结论：在Blbc基础乳腺癌中，我们可以假设FRAT2是潜在的治疗目标。

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