L1CAM promotes epithelial to mesenchymal transition and formation of cancer initiating cells in human endometrial cancer

被引：47
作者：
Chen, Jinlong [1 ]
Gao, Fufeng [1 ]
Liu, Naifu [1 ]
机构：
[1] Shandong Univ, Shandong Canc Hosp, Shandong Acad Med Sci, Dept Gynecol Oncol, 440 Jiyan Rd, Jinan 250117, Shandong, Peoples R China
来源：
EXPERIMENTAL AND THERAPEUTIC MEDICINE | 2018年 / 15卷 / 03期
关键词：
endometrial cancer; cancer initiating cells (CICs); epithelial to mesenchymal transition (EMT); L1CAM; paclitaxel resistance; TUMOR-SUPPRESSOR GENE; ADHESION MOLECULE L1; STEM-CELLS; CYCLOPHILIN-A; MCF-7; CELLS; PANCREATIC-CANCER; IN-VIVO; N-CAM; EXPRESSION; PROLIFERATION;
D O I：
10.3892/etm.2018.5747
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Identification of novel factors critical for epithelial to mesenchymal transition (EMT) and cancer initiating cell (CIC) formation may aid in the identification of novel therapeutics for the treatment of endometrial cancer. The present study demonstrated that L1 cell adhesion molecule (CAM) is critical for EMT and formation of CICs in endometrial cancer. Overexpression of L1CAM may promote EMT with increased formation of CICs in HEC-1A endometrial cancer cells. CICs and mesenchymal status resist chemotherapeutic drugs and may regenerate the various cell types in tumors, thereby resulting in relapse of the disease. The present study demonstrated that overexpressing L1CAM promoted paclitaxel resistance and regulated paclitaxel resistance-associated microRNA expression in HEC-1A cells. Furthermore, it was demonstrated that overexpressing L1CAM promoted anoikis resistance in HEC-1A cells. This link between L1CAM and EMT/CICs may provide a novel target for advancing anticancer therapy.
引用
收藏
页码：2792 / 2797
页数：6
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