and spliced transcripts play an oncogenic role in colorectal carcinogenesis.

Cancer is fundamentally a genetic disorder that alters cellular information flow toward aberrant growth. The coding part accounts for less than 2% of the human genome, and it has become apparent that aberrations within the noncoding genome drive important cancer phenotypes. The numerous carcinogenesis-related genomic variations in the 8q24 region include single nucleotide variations (SNVs), copy number variations (CNVs), and viral integrations occur in the neighboring areas of the locus. It seems that is not the only target of these alterations. The -proximal mutations may act regulatory noncoding RNAs (ncRNAs). In this study, gene expression analyses indicated that the expression of some spliced linear transcripts, , , and is increased in colorectal cancer (CRC). Moreover, the expression of these genes is associated with some clinicopathological characteristics of CRC. Also, studies in CRC cell lines demonstrated that is mostly detected in the nucleus, and different transcripts of have different preferences for nuclear and cytoplasmic parts. Furthermore, perturbation of expression and concomitant perturbation in and expression caused overexpression. It seems that transcription of is under regulatory control at the transcriptional level, i.e., initiation and elongation of transcription by its neighboring genes. Altogether, the current data provide evidence for the notion that these noncoding transcripts can significantly participate in the regulation network and in the carcinogenesis of colorectal cells.