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
. 2017 Jul 23;7(13):3243-3259.
doi: 10.7150/thno.19934. eCollection 2017.

Targeting MicroRNAs in Prostate Cancer Radiotherapy

Affiliations
Review

Targeting MicroRNAs in Prostate Cancer Radiotherapy

Jie Ni et al. Theranostics. .

Abstract

Radiotherapy is one of the most important treatment options for localized early-stage or advanced-stage prostate cancer (CaP). Radioresistance (relapse after radiotherapy) is a major challenge for the current radiotherapy. There is great interest in investigating mechanisms of radioresistance and developing novel treatment strategies to overcome radioresistance. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level, participating in numerous physiological and pathological processes including cancer invasion, progression, metastasis and therapeutic resistance. Emerging evidence indicates that miRNAs play a critical role in the modulation of key cellular pathways that mediate response to radiation, influencing the radiosensitivity of the cancer cells through interplaying with other biological processes such as cell cycle checkpoints, apoptosis, autophagy, epithelial-mesenchymal transition and cancer stem cells. Here, we summarize several important miRNAs in CaP radiation response and then discuss the regulation of the major signalling pathways and biological processes by miRNAs in CaP radiotherapy. Finally, we emphasize on microRNAs as potential predictive biomarkers and/or therapeutic targets to improve CaP radiosensitivity.

Keywords: MicroRNAs; Prostate cancer; Radioresistance; Radiotherapy; Signalling pathway..

PubMed Disclaimer

Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
An overview of roles of miRNAs as a regulator of DDR in response to radiation in cancers. When SSB or DSB occurs, DNA damage repair pathway is initiated. This pathway contains a cascade of components including sensors (MRN and PAPR-1), transducers (ATM and ATR) and effectors (DNA-PK, RAD51 and BRCA1/2), in order to achieve DNA damage repair through NHEJ and HR pathways. Multiple miRNAs play important roles in up-regulating or down-regulating these biological processes in cancer radiation response. ATM, ataxia telangiectasia mutated; ATR, ataxia telangiectasia and Rad3-related protein; DNA-PK, DNA-dependent protein kinase; DSB, double-strand breaks; HR, homologous recombination; IR, irradiation; MRN, MRE11/RAD50/NBS1; NHEJ, non-homologous end joining; PARP-1, Poly [ADP-ribose] polymerase 1; SSB, single-strand breaks. '' indicates down-regulation and '' indicates up-regulation.
Figure 2
Figure 2
An overview of roles of miRNAs as a regulator of cell cycle and apoptosis in radiation response in cancers including CaP. Following the induction of DNA damage by radiation, the reaction that initiates the G1/S or G2/M cell cycle checkpoints is phosphorylation of CHK1 and CHK2 by ATM or ATR. Cell cycle progression is then interrupted to allow time for DNA damage repair by targeting the Cyclin/CDKs complexes whereby affect other components in cell cycle including CDC25, p53 and p21, in order to achieve cell cycle arrest and apoptosis. Multiple miRNAs play important roles in up-regulating or down-regulating these biological processes. CDK, cyclin-dependent kinase; CHK, checkpoint kinase; MCL1, myeloid cell leukaemia 1; SGPP1, sphingosine-1-phosphate phosphatase 1; '⊣' indicates down-regulation and '⟶' indicates up-regulation.

Similar articles

Cited by

References

    1. Siegel RL, Miller KD, Jemal A. Cancer Statistics, 2017. CA Cancer J Clin. 2017;67:7–30. - PubMed
    1. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011;61:69–90. - PubMed
    1. Li L, Story M, Legerski RJ. Cellular responses to ionizing radiation damage. Int J Radiat Oncol Biol Phys. 2001;49:1157–62. - PubMed
    1. Soffen EM, Hanks GE, Hunt MA, Epstein BE. Conformal static field radiation therapy treatment of early prostate cancer versus non-conformal techniques: a reduction in acute morbidity. Int J Radiat Oncol Biol Phys. 1992;24:485–8. - PubMed
    1. Ling CC, Burman C, Chui CS, Kutcher GJ, Leibel SA, LoSasso T. et al. Conformal radiation treatment of prostate cancer using inversely-planned intensity-modulated photon beams produced with dynamic multileaf collimation. Int J Radiat Oncol Biol Phys. 1996;35:721–30. - PubMed

Publication types