OBJECTIVE: To screen long non-coding RNA which influences radiosensitivity of 
colorectal carcinoma cell lines and investigate the mechanism.
METHODS: Under different doses of radiation, colony formation assay and 
single-hit multi-target model were conducted to draw dose-survival curve and SF2 
value of colorectal carcinoma cell lines(RKO, Lovo) was calculated. 
High-throughput lncRNA/mRNA chips were used to screen lncRNA genes and protein 
coding genes with expression differences more than 2 folds between RKO, Lovo 
cell lines and RKO cell line receiving 2Gy radiation. The main action pathway 
was computed by Gene Ontology analysis combined with Pathway analysis in order 
to explore the mechanism which induces the effect of lncRNA on radiosensitivity 
of colorectal carcinoma cell lines. Further experiment on P53, P21, cyclin D1 
expression contents of RKO cell line was confirmed by real-time RT-PCR.
RESULTS: Lovo(SF2=0.47) was more sensitivity to radiation than RKO(SF2=0.53) 
according to the outcome of colony formation assay. High-throughput lncRNA/mRNA 
chips identified a total of 268 lncRNA genes and 270 protein coding genes. Gene 
Ontology analysis showed that the expression of genes associated with cell cycle 
process were significantly different (38.6%). There was a significant 
relationship between expression of several lncRNAs and CCND1 gene. Real-time 
RT-PCR showed no significant differences of P53 and P21 expression in RKO and 
Lovo cell lines(P>0.05), while cyclin D1 expression of RKO cell line was higher 
than that of Lovo cell lines(P<0.05). After exposed to 2 Gy doses of radiation, 
there was an obvious decrease of cyclin D1 expression in RKO cell lines(P<0.05), 
while P53 and P21 expressions were not different(P>0.05).
CONCLUSION: The possible mechanism is that lncRNAs compose transcription 
compound to combine with CCND1 gene and influence radiosensitivity of colorectal 
carcinoma cell lines by regulating expression of cyclin D1, which is independent 
of P53-P21-cyclin D1 pathway.