10.3389/fonc.2019.01383.s006
Lv Lv
Lv
Lv
Liang He
Liang
He
Shaohua Chen
Shaohua
Chen
Yaqun Yu
Yaqun
Yu
Guosong Che
Guosong
Che
Xuan Tao
Xuan
Tao
Shengtao Wang
Shengtao
Wang
Zhiyuan Jian
Zhiyuan
Jian
Xuemei Zhang
Xuemei
Zhang
Table_1_Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression.docx
Frontiers
2019
LINC00114
EZH2
DNMT1
miR-133b
methylation
colorectal cancer
2019-12-24 13:46:07
Dataset
https://frontiersin.figshare.com/articles/dataset/Table_1_Long_Non-coding_RNA_LINC00114_Facilitates_Colorectal_Cancer_Development_Through_EZH2_DNMT1-Induced_miR-133b_Suppression_docx/11449476
<p>This study aimed to identify the roles of the long non-coding RNA LINC00114 in colorectal cancer (CRC) development. The expression levels of LINC00114 and miR-133b in CRC were determined by reverse transcription (RT)-polymerase chain reaction (PCR) and the functions of LINC00114 in CRC were evaluated in vitro and in vivo. Methylation-specific PCR assay was performed to detect the miR-133b promoter methylation in CRC cells. Bioinformatics analysis, RNA immunoprecipitation, dual luciferase assay, RNA pull-down, co-immunoprecipitation (IP), and chromatin IP (ChIP) assays were used to elucidate whether LINC00114 could recruit EZH2/DNMT1 and bind to the miR-133b promoter region, leading to dysregulated methylation and the depression of miR-133b. The expression levels of DNA methyltransferases (DNMTs), EZH2, and nucleoporin 214(NUP214) were analyzed by western blotting. Data showed that LINC00114 was highly expressed, whereas miR-133b was downregulated in the CRC tissues and cells. In vitro, silencing LINC00114 inhibited cell proliferation and impeded cell cycle at the G1/S phase by upregulating miR-133b. In vivo, LINC00114 knockdown reduced tumor growth. Further analysis showed that the methylation in miR-133b promoter region was increased in the CRC and silencing LINC00114 increased miR-133b expression through depressing methylation of its promoter region. ChIP-PCR experiments demonstrated that EZH2 and DNMT1 could bind to the miR-133b promoter region and it was abolished by LINC00114 knockdown. sh-EZH2 reversed the overexpression of DNMTs and CRC cell cycle progression induced by the LINC00114 upregulation. LINC00114 could regulate the NUP214 protein expression by sponging miR-133b. These results demonstrated that LINC00114 suppressed miR-133b expression via EZH2/DNMT1-mediated methylation of its promoter region, indicating that LINC00114 might be a potential novel target for CRC diagnosis and treatment.</p>