Original Article
Long non-coding RNA IQCJ-SCHIP1 antisense RNA 1 is downregulated in colorectal cancer and inhibits cell proliferation
Abstract
Background: IQCJ-SCHIP1 antisense RNA 1 (IQCJ-SCHIP1-AS1) was a functional novel long non-coding RNA (lncRNA) revealed by our previous expression profile. In this study, we aim to investigate its clinical relevance and biological significance in colorectal cancer (CRC).
Methods: We measured the expression levels of IQCJ-SCHIP1-AS1 in 86 paired CRC tissues using quantitative RT-PCR assay, and then analyzed its association with patient prognoses. Moreover, gain-of-function and loss-of-function studies were performed to examine the biological functions of IQCJ-SCHIP1-AS1. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA) were used to elucidate potential mechanisms of IQCJ-SCHIP1-AS1 in CRC.
Results: More than 2-fold decreased expression of IQCJ-SCHIP1-AS1 was found in half of CRC tissues (53.5%, 46/86). IQCJ-SCHIP1-AS1 down-regulation was correlated with poor differentiation (P=0.025), advanced depth of tumor (P=0.022), lymphatic invasion (P=0.010), advanced tumor stage (P=0.006), and poor prognosis (P=0.0027) in CRC patients. The Cox proportional hazards model demonstrated that IQCJ-SCHIP1-AS1 expression was an independent prognostic factor for CRC (HR =0.247, 95% CI: 0.081–0.752, P=0.014). Moreover, knockdown of IQCJ-SCHIP1-AS1 promoted CRC cell proliferation through increasing cell cycle progression and impairing cell apoptosis. Additionally, bioinformatics analysis showed that differential expression genes in IQCJ-SCHIP1-AS1-depleted CRC cells were enriched in the pathways of cell cycle, DNA replication, and p53.
Conclusions: Our results demonstrate that IQCJ-SCHIP1-AS1 has an indicative tumor suppressor role and appears to be a potential prognostic factor in CRC for the first time.
Methods: We measured the expression levels of IQCJ-SCHIP1-AS1 in 86 paired CRC tissues using quantitative RT-PCR assay, and then analyzed its association with patient prognoses. Moreover, gain-of-function and loss-of-function studies were performed to examine the biological functions of IQCJ-SCHIP1-AS1. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA) were used to elucidate potential mechanisms of IQCJ-SCHIP1-AS1 in CRC.
Results: More than 2-fold decreased expression of IQCJ-SCHIP1-AS1 was found in half of CRC tissues (53.5%, 46/86). IQCJ-SCHIP1-AS1 down-regulation was correlated with poor differentiation (P=0.025), advanced depth of tumor (P=0.022), lymphatic invasion (P=0.010), advanced tumor stage (P=0.006), and poor prognosis (P=0.0027) in CRC patients. The Cox proportional hazards model demonstrated that IQCJ-SCHIP1-AS1 expression was an independent prognostic factor for CRC (HR =0.247, 95% CI: 0.081–0.752, P=0.014). Moreover, knockdown of IQCJ-SCHIP1-AS1 promoted CRC cell proliferation through increasing cell cycle progression and impairing cell apoptosis. Additionally, bioinformatics analysis showed that differential expression genes in IQCJ-SCHIP1-AS1-depleted CRC cells were enriched in the pathways of cell cycle, DNA replication, and p53.
Conclusions: Our results demonstrate that IQCJ-SCHIP1-AS1 has an indicative tumor suppressor role and appears to be a potential prognostic factor in CRC for the first time.
