Dicer1 dysfunction promotes stemness and aggression in endometrial carcinoma.
Dicer1 dysfunction promotes stemness and aggression in endometrial carcinoma.
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Dicer1功能障碍促进子宫内膜癌的干性和攻击性
DOI：
10.1177/1010428317695967
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
Wan Xiao Ping
中科院分区：
文献类型：
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作者：
Wang Xiao Jun;Jiang Fei Zhou;Tong Huan;Ke Jie Qi;Li Yi Ran;Zhang Hui Lin;Yan Xiao Fang;Wang Fang Yuan;Wan Xiao Ping
子宫内膜癌是最常见的妇科恶性肿瘤之一，但其发生发展的分子机制尚不清楚。Dicer 1和癌症干细胞在细胞运动和存活中起重要作用。本研究探讨let-7家族和Dicer 1在子宫内膜癌细胞干细胞性中的作用。我们分析了临床样本中Dicer 1的表达，并探讨了其与干细胞相关标志物和临床参数的关系。我们发现Dicer 1功能障碍导致肿瘤干细胞特征和肿瘤侵袭性的富集，无论是在体外还是在体内。我们还确定了与这种潜在的肿瘤易感表型相关的机制：Dicer 1的缺失诱导let-7家族的异常表达，该家族包括众所周知的肿瘤抑制因子，从而调节子宫内膜癌细胞的干性。
Endometrial carcinoma is one of the most common gynecological malignancies, but the molecular events involved in the development and progression of endometrial carcinoma remain unclear. Dicer1 and cancer stem cells play important roles in cell motility and survival. This study investigated the role of the let-7 family and Dicer1 in the stemness of endometrial carcinoma cells. We profiled Dicer1 expression in clinical samples and explored its relationship with stem cell–associated markers and clinical parameters. We showed that Dicer1 dysfunction leads to the enrichment of tumor stemness features and tumor aggression both in vitro and in vivo. We also identified the mechanism related to this potential tumor-predisposing phenotype: loss of Dicer1 induced abnormal expression of the let-7 family, which comprises well-known tumor suppressors, thus regulating stemness in endometrial carcinoma cells.