Long non-coding RNA LOC283070 mediates the transition of LNCaP cells into androgen-independent cells possibly via CAMK1D
Long non-coding RNA LOC283070 mediates the transition of LNCaP cells into androgen-independent cells possibly via CAMK1D
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长非编码RNA LOC283070可能通过CAMK1D介导LNCaP细胞向雄激素非依赖性细胞的转变
DOI：
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发表时间：
2016
期刊：
影响因子：
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通讯作者：
Anli Jiang
中科院分区：
文献类型：
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作者：
Lina Wang;Yani Lin;Hui Meng;Chunyan Liu;Jing Xue;Qi Zhang;Chaoyang Li;Pengju Zhang;Fuai Cui;Weiwen Chen;Anli Jiang
目的：本研究旨在探讨长非编码RNA(LncRNAs)在前列腺癌雄激素非依赖性发生发展中的作用及其机制。方法：从雄激素依赖型前列腺癌(ADPC)细胞系LNCaP中建立雄激素非依赖性前列腺癌(AIPC)细胞系LNCaP-AI。应用基因芯片技术研究LNCaP和LNCaP-AI细胞中LncRNAs和mRNAs的表达谱差异。用实时定量聚合酶链式反应检测RNA的表达。用Western blotting检测蛋白质水平。用四甲基偶氮唑盐比色法检测细胞存活率。采用裸鼠成瘤实验检测肿瘤的体内生长情况。流式细胞仪检测细胞周期。Transwell法检测细胞迁移和侵袭能力。结果：根据生物信息学预测，LncRNA LOC283070可能在LNCaP细胞向LNCaP-AI细胞转化过程中发挥重要作用。LOC283070在LNCaP-AI细胞中高表达，在AIPC细胞中高表达。LOC283070在LNCaP细胞中的过表达加速了细胞的增殖和迁移，即使在雄激素非依赖性的环境中也是如此。LOC283070基因敲除可抑制LNCaP-AI细胞的增殖和迁移。此外，LOC283070的过表达促进了正常小鼠和去势小鼠体内肿瘤的生长。CAMK1D过表达与LOC283070的作用相似，CAMK1D基因敲除可完全阻断LOC283070过表达对LNCaP细胞向雄激素非依赖性细胞转化的影响。结论：LOC283070过表达可能通过CAMK1D介导LNCaP细胞向雄激素非依赖性LNCaP-AI细胞的转化。
Aims: The present study is to investigate the role of long non-coding RNAs (lncRNAs) in the development of androgen independence in prostate cancer and its underlying mechanism. Methods: We established an androgen-independent prostate carcinoma (AIPC) cell line LNCaP-AI from androgen-dependent prostate carcinoma (ADPC) cell line LNCaP. Different expression profiles of lncRNAs and mRNAs between LNCaP and LNCaP-AI cells were investigated using microarray analysis. The expression of RNAs was determined using quantitative real-time polymerase chain reaction. Protein levels were measured using Western blotting. MTT assay was used to test cell viability. Tumor formation assay was performed in nude mice to detect tumor growth in vivo. Flow cytometry was performed to detect cell cycles. Transwell assay was employed to test cell migration and invasion. Results: According to bioinformatics prediction, lncRNA LOC283070 could possibly play an important role in the transition of LNCaP cells into LNCaP-AI cells. LOC283070 was up-regulated in LNCaP-AI cells and frequently up-regulated in AIPC cell lines. Overexpression of LOC283070 in LNCaP cells accelerated cell proliferation and migration, even under androgen-independent circumstances. Knockdown of LOC283070 inhibited LNCaP-AI cell proliferation and migration. Moreover, overexpression of LOC283070 promoted tumor growth in vivo in both normal mice and castrated mice. CAMK1D overexpression had similar effect with LOC283070, and CAMK1D knockdown fully abrogated the effect of LOC283070 overexpression on the transition of LNCaP cells into androgen-independent cells. Conclusions: The present study shows that overexpression of LOC283070 mediates the transition of LNCaP cells into androgen-independent LNCaP-AI cells possibly via CAMK1D.