Abstract
Long non-coding RNAs (lncRNAs) are participated in tumourigenesis, including colorectal cancer (CRC). However, the effects and mechanisms of lncRNA POU6F2-AS1 in CRC have not been investigated. KIAA1429 act as a member of N6-methyladenosine (m6A) modification, has been knew as an oncogenic factor in various cancer containing CRC. We focus to investigate the regulation effect of lncRNA POU6F2-AS1, and the mechanism among lncRNA POU6F2-AS1 and KIAA1429 in CRC. The lncRNA POU6F2-AS1 and KIAA1429 levels in CRC tissue samples as well as cells were clarified by qRT-PCR, and their relationship was predicted by bioinformatics, MeRIP and Pearson analysis. Cell survival, migration and invasion were analyzed via EdU, wound healing and Transwell assays after lncRNA POU6F2-AS1 was down-regulated and KIAA1429 was up-regulated. LncRNA POU6F2-AS1 and KIAA1429 were enriched in CRC tissue samples. LncRNA POU6F2-AS1 silencing suppressed CRC cell survival, migration, and invasion, and KIAA1429 overexpression facilitated CRC cell malignancy. KIAA1429 promoted lncRNA POU6F2-AS1 expression via m6A modification. Furthermore, KIAA1429 upregulation reversed the inhibitory effect of lncRNA POU6F2-AS1 interference on the malignant behavior of CRC cells. lncRNA POU6F2-AS1 was modulated by KIAA1429 in the form of m6A modification to regulate the malignant phenotype of CRC, which may provide new insights into the potential application of KIAA1429-m6A-lncRNA POU6F2-AS1-based CRC therapy.

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