Mechanisms of radioresistance and the underlying signaling pathways in colorectal cancer cells

被引:8
作者
Tessmann, Josiane W. [1 ]
Rocha, Murilo R. [1 ,2 ]
Morgado-Diaz, Jose A. [1 ,2 ]
机构
[1] Brazilian Natl Canc Inst INCA, Cellular & Mol Oncobiol Program, Rio De Janeiro, Brazil
[2] Brazilian Natl Canc Inst INCA, Cellular & Mol Oncobiol Program, 37 Andre Cavalcanti St,3th Floor, BR-20231050 Rio De Janeiro, RJ, Brazil
关键词
autophagy; cancer stem cells; colorectal cancer; epithelial-mesenchymal transition; polyploid giant cancer cells; radioresistance; EPITHELIAL-MESENCHYMAL TRANSITION; DNA-DAMAGE RESPONSE; IONIZING-RADIATION; THERAPEUTIC TARGET; STEM-CELLS; AUTOPHAGY; RESISTANCE; SENESCENCE; RADIOSENSITIVITY; RADIOTHERAPY;
D O I
10.1002/jcb.30361
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Radiotherapy is one of the most common modalities for the treatment of a wide range of tumors, including colorectal cancer (CRC); however, radioresistance of cancer cells remains a major limitation for this treatment. Following radiotherapy, the activities of various cellular mechanisms and cell signaling pathways are altered, resulting in the development of radioresistance, which leads to therapeutic failure and poor prognosis in patients with cancer. Furthermore, even though several inhibitors have been developed to target tumor resistance, these molecules can induce side effects in nontumor cells due to low specificity and efficiency. However, the role of these mechanisms in CRC has not been extensively studied. This review discusses recent studies regarding the relationship between radioresistance and the alterations in a series of cellular mechanisms and cell signaling pathways that lead to therapeutic failure and tumor recurrence. Our review also presents recent advances in the in vitro/in vivo study models aimed at investigating the radioresistance mechanism in CRC. Furthermore, it provides a relevant biochemical basis in theory, which can be useful to improve radiotherapy sensitivity and prolong patient survival.
引用
收藏
页码:31 / 45
页数:15
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