Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Jul 22:12:889658.
doi: 10.3389/fonc.2022.889658. eCollection 2022.

Role of non-coding RNAs in radiosensitivity of colorectal cancer: A narrative review

Chun-Ming Huang  1   2   3   4 , Hsiang-Lin Tsai  5   6 , Yen-Cheng Chen  5   7 , Ching-Wen Huang  5   6 , Ching-Chun Li  5 , Wei-Chih Su  5   7 , Tsung-Kun Chang  5   6 , Yung-Sung Yeh  8   9   10 , Po-Jung Chen  5 , Ming-Yii Huang  2   3   11 , Jaw-Yuan Wang  4   5   6   7   11   12
Affiliations
Review

Role of non-coding RNAs in radiosensitivity of colorectal cancer: A narrative review

Chun-Ming Huang et al. Front Oncol. .

Abstract

Colorectal cancer (CRC) is a global public health concern because of its high prevalence and mortality. Although radiotherapy is a key method for treating CRC, radioresistance is an obstacle to radiotherapy use. The molecular mechanisms underlying the radioresistance of CRC remain unclear. Increasing evidence has revealed the multiple regulatory functions of non-coding RNAs (ncRNAs) in numerous malignancies, including CRC. Several ncRNAs have been reported to be involved in the determination of radiosensitivity of CRC cells, and some have excellent potential to be prognostic biomarkers or therapeutic targets in CRC treatment. The present review discusses the biological functions and underlying mechanisms of ncRNAs (primarily lncRNA, miRNA, and circRNA) in the regulation of the radiosensitivity of CRC. We also evaluate studies that examined ncRNAs as biomarkers of response to radiation and as therapeutic targets for enhancing radiosensitivity.

Keywords: biomarkers; colorectal cancer; ncRNAs; radioresistance; radiosensitivity.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Mechanisms of ncRNAs contributing to CRC cell radiosensitivity. Radiation induces several types of DNA damage, and double-strand breaks (DSBs) are lethal. DNA damage activates the DNA damage repair pathway and the homologous recombination (HR) and the non-homologous end joining (NHEJ) are the most classic mechanisms for DSB repair. DNA damage repair results in two pathways: apoptosis and DNA repair, which lead to radiosensitivity or radioresistance. LncRNAs and circRNAs downregulate the expression levels of miRNA-targeted mRNAs by sponging their targeted miRNAs. mRNAs can directly regulate the DNA damage repair and indirectly modulate repair mechanisms through several onco-signaling pathways, such as Wnt/β-catenin, epithelial-mesenchymal transition (EMT), and DNA damage response. Taken together, the lncRNA-miRNA-mRNA and circRNA-miRNA-mRNA interaction networks modulate the radiosensitivity of CRC cells by regulating DNA damage repair pathways.
Figure 2
Figure 2
Schematic depicting several pathways of ncRNAs in modulating radiation response to CRC cells. (A) Several ncRNAs regulate radiosensitivity by targeting insulin-like growth factor receptor signaling pathways. (B) A few ncRNAs modulate cell apoptosis by regulating anti-apoptotic pathways. (C) Some ncRNAs modulate response to irradiation by mediating autophagy pathways. (D) Many ncRNAs manipulate epithelial-mesenchymal transition (EMT) by enhancing EMT (e.g., TLCD2-1) or inhibiting EMT (e.g., miR-124). (E) Numerous ncRNAs regulate DNA damage response pathways (e.g., p53 pathways) to modulate radiosensitivity. (F) Specific ncRNAs control NF-κB signaling pathways to overcome radioresistance. (G) Some ncRNAs mediate cellular response to irradiation via targeting Wnt/β-catenin. (H) Several ncRNAs regulate radiosensitivity through mediating DNA damage repair pathways, such as non-homologous end joining (NHEJ).
See this image and copyright information in PMC

References

    1. Keum N, Giovannucci E. Global burden of colorectal cancer: Emerging trends, risk factors and prevention strategies. Nat Rev Gastroenterol Hepatol (2019) 16(12):713–32. doi: 10.1038/s41575-019-0189-8 - DOI - PubMed
    1. Arnold M, Sierra MS, Laversanne M, Soerjomataram I, Jemal A, Bray F. Global patterns and trends in colorectal cancer incidence and mortality. Gut (2017) 66(4):683–91. doi: 10.1136/gutjnl-2015-310912 - DOI - PubMed
    1. Schreuders EH, Ruco A, Rabeneck L, Schoen RE, Sung JJ, Young GP, et al. Colorectal cancer screening: A global overview of existing programmes. Gut (2015) 64(10):1637–49. doi: 10.1136/gutjnl-2014-309086 - DOI - PubMed
    1. Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: Globocan estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: Cancer J Clin (2018) 68(6):394–424. doi: 10.3322/caac.21492 - DOI - PubMed
    1. van Gijn W, Marijnen CA, Nagtegaal ID, Kranenbarg EM, Putter H, Wiggers T, et al. Preoperative radiotherapy combined with total mesorectal excision for resectable rectal cancer: 12-year follow-up of the multicentre, randomised controlled tme trial. Lancet Oncol (2011) 12(6):575–82. doi: 10.1016/s1470-2045(11)70097-3 - DOI - PubMed

LinkOut - more resources