Abstract
Colorectal cancer (CRC) is responsible for one of the major cancer incidence and mortality worldwide. It is well known that MicroRNAs (miRNAs) play vital roles in maintaining the cell development and other physiological processes, as well as, the aberrant expression of numerous miRNAs involved in CRC progression. MiRNAs are a class of small, endogenous, non-coding, single-stranded RNAs that bind to the 3’-untranslated region (3′-UTR) complementary sequences of their target mRNA, resulting in mRNA degradation or inhibition of its translation as a post-transcriptional regulators. Moreover, miRNAs also can target the long non-coding RNA (lncRNA) to regulate the expression of its target genes involved in proliferation and metastasis of CRC. The functions of these dysregulated miRNAs appear to be context specific, with evidence of having a dual role in both oncogenes and tumor suppression depending on the cellular environment in which they are expressed. Therefore, the unique expression profiles of miRNAs relate to the diagnosis, prognosis, and therapeutic outcome in CRC. In this review, we focused on several oncogenic and tumor-suppressive miRNAs specific to CRC, and assess their functions to uncover the molecular mechanisms of tumor initiation and progression in CRC. These data promised that miRNAs can be used as early detection biomarkers and potential therapeutic target in CRC patients.
Highlights
Colorectal cancer (CRC) is the third leading cause of cancer related mortality in both men and women, with an incidence approaching over 1.4 million people and about 693,900 deaths annually [1]
Substantial progress has revealed the relationship between miRNAs and CRC, where miRNAs were proved to participate in multiple biological processes, such as cell cycle, apoptosis, invasion, migration, and metastasis in CRC
We focused on several microRNAs shown to be specific to CRC, their roles in CRC biology was summarized in association with molecular processes underlying carcinogenesis and progression of CRC
Summary
Colorectal cancer (CRC) is the third leading cause of cancer related mortality in both men and women, with an incidence approaching over 1.4 million people and about 693,900 deaths annually [1]. 5-FU is non-specific and CRC is resistant to it Adjuvant chemotherapy, such as 5-FU plus leucovorin (LV) (5-FU/LV), infusional 5-FU, LV, oxaliplatin (FOLFOX), tegafur plus uracil (UFT), or capecitabine have been developed and are widely used against the CRC [8]. The key enzymes, such as thymidylate synthase (TS), thymidine phosphorylase (TP), orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD) were used as predictive biomarkers of the efficacy of 5-FU chemotherapy and targeted therapy in CRC cells [9]. Many reports showed that the mutations of the target genes or the downstream signaling molecules greatly reduced their efficiency or even caused the clinical treatment to be inactivated [12]
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