Background and purpose: Accumulating evidence has revealed that long non-coding RNA (lncRNA) is correlated with carcinogenesis and tumor development. Recent literature suggested that lncRNA promoter of CDKN1A antisense DNA damage activated RNA (PANDAR) was involved in the development of various cancers. However

the functional role of PANDAR in colorectal cancer (CRC) has not been elucidated yet. The present study aimed to explore the functional role of lncRNA PANDAR in promoting CRC metastasis and its mechanism. Methods: The expression of lncRNA PANDAR in CRC cell lines and tissues was detected by real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR)

and the correlation between lncRNA PANDAR expression and CRC clinicopathological characteristics was statistically analyzed. Then

lncRNA PANDAR stably silencing CRC cells (HCT116-shPANDAR)

overexpression cells (DLD1-PANDAR) and control vector cells (HCT116-shNC and DLD1-vector) were established using lentiviral vectors. Moreover

Transwell assay and Matrigel assay were performed to investigate the function of lncRNA PANDAR in CRC migration and invasion. Furthermore

the expression of transcriptional factors mediating epithelial-mesenchymal transition of lncRNA PANDAR overexpression cells were monitored by RTFQ-PCR assay

and the function of the target gene in modulating lncRNA PANDAR mediated CRC metastasis was also explored. Results: The expression levels of lncRNA PANDAR in normal colorectal epithelial cells were much lower than in CRC cell. The levels of lncRNA PANDAR in tumor-adjacent tissues were verified to be much lower than in CRC tissues ［(171.52±97.80)% vs (100.00±63.18)%

P0.05］. Moreover

the expression of lncRNA PANDAR was detected to be significantly correlated with CRC TNM stage

lymph node metastasis and distant metastasis (P0.05). Besides

lncRNA PANDAR deficiency significantly reduced the migration ［100.00% vs (42.08±4.77)%

P0.05］ and invasion ［100.00% vs (39.14±3.81)%

P0.05］ capabilities in CRC cells

in contrast

the migration ［100.00% vs (194.12±9.33)%

P0.05］ and invasion ［100.00% vs (204.08±12.27)%

P0.05］ capabilities of CRC cells were obviously increased with lncRNA PANDAR overexpression. Furthermore

zinc-finger E-box binding homeobox 1 (ZEB1) expression was detected to be positively correlated with lncRNA PANDAR expression

and ZEB1 silencing could significantly reverse the increased migration and invasion capabilities induced by lncRNA PANDAR in CRC cells. Conclusion: LncRNA PANDAR could promote CRC metastasis by potentially targeting ZEB1. LncRNA PANDAR might be a promising diagnostic marker and therapeutic target for CRC patients.