Abstract
Colorectal cancer (CRC) is the third most frequent cancer and one of the leading causes for cancer-related mortality. Aberrant activation of the Wnt signaling is an essential initiating factor in colon carcinogenesis, and a driving force of CRC progression. Recently, long non-coding RNAs (lncRNAs) have emerged as significant players in CRC pathogenesis through diversified mechanisms. Although both Wnt signaling and lncRNAs represent interesting research areas for CRC, an effort of directly connecting these two areas is lacking. To fill in the knowledge gap, we focus on the reported findings of lncRNAs that regulate Wnt signaling or essential Wnt signaling targets. These include several newly discovered lncRNAs originated from the amplified cancer-associated chromosome 8q24 region that surrounds the essential Wnt target MYC gene, lncRNAs reported to be involved in CRC stem cells, and several individual lncRNAs connected to Wnt signaling through other mechanisms. This review will provide essential information that assists in understanding the missing link of lncRNAs to the classical Wnt signaling in CRC.
Highlights
Colorectal cancer (CRC), accounting for 8% of new cancer cases, is the third most frequent cancer, and one of the leading cause of cancer-related mortalities in the United States [1]
As an essential signaling in CRC initiation and progression, Wnt signaling is involved in all key aspects of cancer biology related to tumor growth, metastasis, and therapeutic response
The emerging concept of long non-coding RNAs (lncRNAs) as important players in CRC by regulating Wnt singling deserves the attention of both academia and the biotechnological industry
Summary
Colorectal cancer (CRC), accounting for 8% of new cancer cases, is the third most frequent cancer, and one of the leading cause of cancer-related mortalities in the United States [1]. As an initiating event in both familial adenomatous polyposis and sporadic CRCs [20,21], the mutational inactivation of APC leads to the accumulation of β-catenin in the nucleus, a hallmark of the canonical Wnt signaling, and the transcriptional activation of Wnt target genes by β-catenin/TCF complex [22,23]. Restoration of APC reverted CRC tumorigenic lesions by re-establishing the normal crypt homeostasis, even in mice harboring oncogenic Kras and mutated p53 [25] This experimental finding reinforces the essential suppressor function of APC in CRC initiation, and revealed the critical importance of APC-regulated Wnt signaling in CRC progression. As classical downstream targets that respond to Wnt signaling, CCND1 and MYC are established drivers in CRC formation by regulating cell growth, apoptosis, migration, invasion and stem cell maintenance [26,27]
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