This review article deals with comprehensive information about the evolutionary history of introns with their localization and functions in the gene transcripts of colorectal cancer precisely. In this way, the major breakthrough in the molecular biology discipline was the discovery of introns by Richard Robert and Phil Sharp in 1977. Firstly, noncoding regions are recognized by various assortments of regulatory ncRNA sequences such as circular RNA, telomere-associated RNA, small nuclear RNA, Piwi-interacting RNA, small interfering RNA, small nucleolar RNA, microRNA, and long noncoding RNA. Fortunately, splicing process of mRNA strand deals with the excision of introns via spliceosomal proteins into mature mRNA which is witnessed only in eukaryotic organisms and devoid of the splicing machinery components in the prokaryotic organisms. The major focal point relies on intronic genes mainly involved in the progression of colorectal cancer with preliminary information. An alternative splicing process takes place in mRNA that implicates in intron retention leading to varied gene expression in cells and tissues and their promotion in colorectal cancer. Therefore, colorectal cancer-associated diseases have paved the way to know more about the intronic genes mainly concentrated among them in the progression of the related diseases. Hence, the focus of the researchers is toward the fascinating cellular and molecular biology aspects of the regulatory intronic sequences known to enhance as well as repress particular gene expression in tumor microenvironment of colorectal cancer by analyzing the genome and proteome levels for the betterment of human kind that is intended for various therapeutic purposes.
Introns (noncoding sequences) mRNA Spliceosomal proteins Alternate splicing process Intron retention Colorectal cancer
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The authors are thankful to Science and Engineering Research Board (SERB) (EMR/20l7/001877) for providing the Core Research Grant to Prof. Surajit Pathak and Chettinad Academy of Research and Education for the research support.
Niu D-K, Yang Y-F (2011) Why eukaryotic cells use introns to enhance gene expression: splicing reduces transcription associated mutagenesis by inhibiting topoisomerase I cutting activity. Biol Direct 6:24CrossRefGoogle Scholar
Jeffares DC, Mourier T, Penny D (2006) The biology of intron gain and loss. Trends Genet 22(1):16–22CrossRefGoogle Scholar
Haugen P, Simon DM, Bhattacharya D (2005) The natural history of group I introns. Trends Genet 21(2):111–119CrossRefGoogle Scholar
Irimia M, Roy SW (2014) Origin of spliceosomal introns and alternative splicing. Cold Spring Harb Perspect Biol 6(6):a016071CrossRefGoogle Scholar
Middleton R, Gao D, Thomas A et al (2017) Irfinder: assessing the impact of intron retention on mammalian gene expression. Genome Biol 18(1):51CrossRefGoogle Scholar
Esquela-Kerscher A, Slack FJ (2006) Oncomirs – microRNAs with a role in cancer. Nat Rev Cancer 6(4):259–269CrossRefGoogle Scholar
Lizarbe MA, Fernández-Lizarbe S, Calle-Espinosa J et al (2017) Colorectal cancer: from the genetic model to posttranscriptional regulation by noncoding RNAs. Hindawi Biomed Res Int 2017:7354260Google Scholar
Cheetham SW, Gruhl F, Mattick JS, Dinger ME (2013) Long noncoding rnas and the genetics of cancer. Br J Cancer 108:2419–2425CrossRefGoogle Scholar
Alhopuro P, Sammalkorpi H et al (2011) Candidate driver genes in microsatellite-unstable colorectal cancer. Int J Cancer 130(7):1558–1566CrossRefGoogle Scholar
Sameer AS (2013) Colorectal cancer: molecular mutations and polymorphisms. Front Oncol 3:114CrossRefGoogle Scholar
Jung H, Lee D, Lee J et al (2015) Intron retention is a widespread mechanism of tumor-suppressor inactivation. Nat Genet 47(11):1242–1248CrossRefGoogle Scholar
Dvinge H, Bradley RK (2015) Widespread intron retention diversifies most cancer transcriptomes. Genome Med 7:45CrossRefGoogle Scholar
Wong JJ-L, Au AYM et al (2015) Intron retention in mRNA: no longer nonsense. Bioessays 38:41–49CrossRefGoogle Scholar
Fang X et al (2016) SNORD126 promotes HCC and CRC cell growth by activating the PI3K-AKT pathway through FGFR2. J Mol Cell Biol Adv 9(3):243–255Google Scholar