Sensitization of prostate cancer to radiation therapy: Molecules and pathways to target

Mu Yao; Linda Rogers; Natalka Suchowerska; Daniel Choe; Mahmoud A Al-Dabbas; Ramit S Narula; J Guy Lyons; Paul Sved; Zhong Li; Qihan Dong

doi:10.1016/j.radonc.2018.05.021

Sensitization of prostate cancer to radiation therapy: Molecules and pathways to target

Radiother Oncol. 2018 Aug;128(2):283-300. doi: 10.1016/j.radonc.2018.05.021. Epub 2018 Jun 18.

Authors

Mu Yao¹, Linda Rogers², Natalka Suchowerska², Daniel Choe¹, Mahmoud A Al-Dabbas³, Ramit S Narula⁴, J Guy Lyons⁵, Paul Sved⁶, Zhong Li⁷, Qihan Dong⁸

Affiliations

¹ Central Clinical School and Charles Perkins Centre, Australia; Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, Australia.
² Department of Radiation Oncology, Chris O'Brien Lifehouse, Sydney, Australia; School of Physics, University of Sydney, Australia.
³ School of Science and Health, Western Sydney University, Australia.
⁴ School of Science and Health, Western Sydney University, Australia; School of Medicine, Western Sydney University, Australia.
⁵ Central Clinical School and Charles Perkins Centre, Australia; Cancer Services, Royal Prince Alfred Hospital, Sydney, Australia; Immune Imaging Program, Centenary Institute, Sydney, Australia.
⁶ Department of Urology, Bankstown-Lidcombe Hospital, Sydney, Australia.
⁷ Dongzhimen Hospital, Beijing University of Chinese Medicine, China. Electronic address: lee171@163.com.
⁸ Central Clinical School and Charles Perkins Centre, Australia; Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, Australia; School of Science and Health, Western Sydney University, Australia. Electronic address: q.dong@uws.edu.au.

PMID: 29929859
DOI: 10.1016/j.radonc.2018.05.021

Abstract

Radiation therapy is used to treat cancer by radiation-induced DNA damage. Despite the best efforts to eliminate cancer, some cancer cells survive irradiation, resulting in cancer progression or recurrence. Alteration in DNA damage repair pathways is common in cancers, resulting in modulation of their response to radiation. This article focuses on the recent findings about molecules and pathways that potentially can be targeted to sensitize prostate cancer cells to ionizing radiation, thereby achieving an improved therapeutic outcome.

Keywords: DNA damage; DNA repair; Prostate cancer; Radiation.

Publication types

Review

MeSH terms

Ataxia Telangiectasia Mutated Proteins / genetics
Ataxia Telangiectasia Mutated Proteins / radiation effects
Aurora Kinases / radiation effects
Cell Cycle / radiation effects
Checkpoint Kinase 1 / radiation effects
Cyclin-Dependent Kinases / radiation effects
Cyclins / radiation effects
DNA Damage / radiation effects*
DNA Repair / radiation effects*
HSP90 Heat-Shock Proteins / radiation effects
Histone Deacetylases / radiation effects
Humans
Hyaluronan Receptors / radiation effects
Hypoxia-Inducible Factor 1, alpha Subunit / radiation effects
Male
Mutation / radiation effects
NEDD8 Protein / radiation effects
Neoplasm Recurrence, Local / etiology
Neoplasm Recurrence, Local / radiotherapy
Neoplasm, Residual
Neoplastic Stem Cells / radiation effects
Phosphatidylinositol 3-Kinases / radiation effects
Poly(ADP-ribose) Polymerases / radiation effects
Prostatic Neoplasms / radiotherapy*
Proto-Oncogene Proteins c-met / radiation effects
Radiation Tolerance
Radiation, Ionizing
Receptors, Androgen / radiation effects
TOR Serine-Threonine Kinases / radiation effects
Zinc Finger Protein GLI1 / radiation effects

Substances

CD44 protein, human
Cyclins
HIF1A protein, human
HSP90 Heat-Shock Proteins
Hyaluronan Receptors
Hypoxia-Inducible Factor 1, alpha Subunit
NEDD8 Protein
NEDD8 protein, human
Receptors, Androgen
Zinc Finger Protein GLI1
Poly(ADP-ribose) Polymerases
MTOR protein, human
Proto-Oncogene Proteins c-met
Ataxia Telangiectasia Mutated Proteins
Aurora Kinases
Checkpoint Kinase 1
TOR Serine-Threonine Kinases
Cyclin-Dependent Kinases
Histone Deacetylases