长链非编码RNA LINC01116通过调控miR-744-5p/UBE2L3轴在前列腺癌细胞中发挥癌基因作用。
Long non-coding RNA LINC01116 acts as an oncogene in prostate cancer cells through regulation of miR-744-5p/UBE2L3 axis.
作者信息
Yu Shengjie, Yu Huihong, Zhang Yuanfeng, Liu Chuan, Zhang Weili, Zhang Yunyun
机构信息
Department of Urology, The Second Affiliated Hospital, Chongqing Medical University, No. 76 Linjiang Road, Chongqing, 400016, China.
Department of Gastroenterology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400016, China.
出版信息
Cancer Cell Int. 2021 Mar 16;21(1):168. doi: 10.1186/s12935-021-01843-w.
BACKGROUND
Long non-coding RNA (lncRNA) has been confirmed to exert a critical effect on the progression of tumors, including prostate cancer. Previous literature has demonstrated LINC01116 involves in activities of multiple cancers. However, the underlying role of LINC01116 in prostate cancer remains unclear.
METHODS
qRT-PCR measured the expression of LINC01116 in prostate cancer cells. EdU experiment was used to detect cell proliferation. Transwell assays detected cell migration and invasion. Immunofluorescence staining and western blot assays were utilized to measure EMT progress. The binding relationship between RNAs was confirmed by a series of mechanism assays. In addition, rescue experiments were conducted to verify the relationship among RNAs.
RESULTS
LINC01116 was found to be highly expressed in prostate cancer cells. Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. In rescue assays, we discovered that inhibited miR-744-5p or overexpressed UBE2L3 could offset the suppressive influence of silencing LINC01116 on prostate cancer cells.
CONCLUSION
Our study suggested that lncRNA LINC01116 acted as an oncogene in prostate cancer and accelerated prostate cancer cell growth through regulating miR-744-5p/UBE2L3 axis.
背景
长链非编码RNA（lncRNA）已被证实对包括前列腺癌在内的肿瘤进展发挥关键作用。既往文献表明LINC01116参与多种癌症的活动。然而，LINC01116在前列腺癌中的潜在作用仍不清楚。
方法
qRT-PCR检测前列腺癌细胞中LINC01116的表达。EdU实验用于检测细胞增殖。Transwell实验检测细胞迁移和侵袭。免疫荧光染色和蛋白质印迹实验用于测量上皮-间质转化进程。通过一系列机制实验证实RNA之间的结合关系。此外，进行挽救实验以验证RNA之间的关系。
结果
发现LINC01116在前列腺癌细胞中高表达。功能实验表明，抑制LINC01116可抑制细胞增殖、迁移、侵袭和上皮-间质转化进程。此外，已证实miR-744-5p与LINC01116结合。而且，UBE2L3被验证为miR-744-5p的靶基因。在挽救实验中，我们发现抑制miR-744-5p或过表达UBE2L3可抵消沉默LINC01116对前列腺癌细胞的抑制作用。
结论
我们的研究表明，lncRNA LINC01116在前列腺癌中作为癌基因发挥作用，并通过调节miR-744- /UBE2L3轴加速前列腺癌细胞生长。
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