Abstract
Colorectal cancers have become the second leading cause of cancer-related deaths. In particular, acquired chemoresistance and metastatic lesions occurring in colorectal cancer are a major challenge for chemotherapy treatment. Accumulating evidence shows that long non-coding (lncRNAs) are involved in the initiation, progression, and metastasis of cancer. We here discuss the epigenetic mechanisms through which lncRNAs regulate gene expression in cancer cells. In the second part of this review, we focus on the role of lncRNA Urothelial Cancer Associated 1 (UCA1) to integrate research in different types of cancer in order to decipher its putative function and mechanism of regulation in colorectal cancer cells. UCA1 is highly expressed in cancer cells and mediates transcriptional regulation on an epigenetic level through the interaction with chromatin modifiers, by direct regulation via chromatin looping and/or by sponging the action of a diversity of miRNAs. Furthermore, we discuss the role of UCA1 in the regulation of cell cycle progression and its relation to chemoresistance in colorectal cancer cells.
Highlights
Acquired chemoresistance and metastatic lesions occurring in colorectal cancer are a major challenge for chemotherapy treatment
Levels of Urothelial Cancer Associated 1 (UCA1) transcripts are regulated post-transcriptionally; the RNA stability of UCA1 was downregulated by the interaction with insulin-like growth factor 2 messenger RNA binding protein (IMP1) [131] and by the interaction with miR-1 [132], whereas binding of UCA1 to heterogeneous nuclear ribonucleoprotein I increased its stability [133]
The high expression of UCA1 is correlated with a bad cancer prognosis, which is probably related to the induction of chemotherapy drug resistance
Summary
Colon and rectal cancers (together nominated colorectal cancer (CRC)) have become the second leading cause of cancer deaths both in the United States and in Europe ([1,2], respectively). Colon and rectal cancers are frequently analyzed in epidemiological studies as one entity, differences in clinical and molecular characteristics of primary colon cancers were recently re-highlighted between tumors from the right side, including the caecum, ascending colon, hepatic flexure and two-thirds of the transverse colon (~27% of patients), and one from the left-sided colon, including the distal third of the transverse colon, splenic flexure, descending colon, sigmoid and rectum [13,14,15]. This bad prognosis could be due to the acquired cellular chemoresistance and the presence of residual colon cancer cells
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