کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8534676 | 1560522 | 2018 | 30 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuralized1a regulates asymmetric division in mouse Lewis lung carcinoma cells
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
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چکیده انگلیسی
Asymmetric division (ASD), the unique characteristic of normal stem cells, is regarded as a stemness marker when applied to the study of cancer stem cells (CSCs). However, the role of ASD in the self-renewal of CSCs and its regulation remain largely unknown. Here, we first established a mouse Lewis lung carcinoma CSC cell line that could undergo asymmetric division (LLC-ASD cells) derived from the parental mouse Lewis lung carcinoma cancer cells (LLC-Parental cells). In vitro assessment of stemness by RT-qPCR and western blot analysis of stem cell markers, clonogenic assay (pâ¯<â¯0.001), single cell spheroid formation assay (pâ¯<â¯0.05) and 96-well-plate single-cell cloning assay (pâ¯<â¯0.01) indicated that the LLC-ASD cells exhibited stronger stemness features in comparison to the LLC-Parental cells. In vivo, tumorigenicity of LLC-ASD cells, transplanted subcutaneously to the nude mice, was increased compared to that of LLC-parental cells (pâ¯<â¯0.05). Further, Neuralized1a, a regulator of ASD in normal stem cells, was highly expressed in the LLC-ASD cells. Silencing Neuralized1a expression in LLC-ASD cells by siRNA weakened the stemness features measured by the in vitro assays listed above (pâ¯<â¯0.05). The tumorigenic ability was also decreased in the nude mice upon Neuralized1a silencing (pâ¯<â¯0.05). Collectively, the present study suggests that Neuralized1a regulates the stemness of LLC-ASD cells which could be the new marker and therapeutic target of CSCs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Life Sciences - Volume 206, 1 August 2018, Pages 70-76
Journal: Life Sciences - Volume 206, 1 August 2018, Pages 70-76
نویسندگان
Liangsheng Kong, Jingyuan Li, Yongli Liu, Zhiwei Sun, Shixia Zhou, Junling Tang, Ting Ye, Jianyu Wang, H. Rosie Xing,