Radiation induces the generation of cancer stem cells: A novel mechanism for cancer radioresistance

Li, Fengsheng; Zhou, Kunming; Gao, Ling; Zhang, Bin; Li, Wei; Yan, Weijuan; Song, Xian‐Rong; Yu, Hui; Wang, Sinian; Ye, Nan; Jiang, Qisheng

doi:10.3892/ol.2016.5124

Cited by 83 publications

(55 citation statements)

References 99 publications

(110 reference statements)

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“…One of the causes of tumor recurrence and metastasis is that cancer cells acquire radioresistance (RR) during fractionated irradiation (7). It has been reported that RR is acquired in various cancer types, including head and neck cancer, non-small cell lung cancer, breast cancer and PCa (8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Understanding the mechanism underlying the acquisition of radioresistance in human prostate cancer cells

et al. 2019

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Acquisition of radioresistance (RR) has been reported during cancer treatment with fractionated irradiation. However, RR is poorly understood in the prognosis of radiotherapy. Although radiotherapy is important in the treatment of prostate cancer (PCa), acquisition of RR has been reported in PCa with an increased number of cancer stem cells (CSCs), neuroendocrine differentiation (NED) and epithelial-mesenchymal transition. However, to the best of our knowledge, the mechanism underlying RR acquisition during fractionated irradiation remains unclear. In the present study, human PCa cell lines were subjected to fractionated irradiation according to a fixed schedule as follows: Irradiation (IR)1, 2 Gy/day with a total of 20 Gy; IR2, 4 Gy/day with a total of 20 Gy; and IR3, 4 Gy/day with a total of 56 Gy. The expression of cluster of differentiation (CD)44, a CSC marker, was identified to be increased by fractionated irradiation, particularly in DU145 cells. The expression levels of CD133 and CD138 were increased compared with those in parental cells following a single irradiation or multiple irradiations; however, the expression levels decreased with subsequent irradiation. RR was evidently acquired by exposure to 56 Gy radiation, which resulted in increased expression of the NED markers CD133 and CD138, and increased mRNA expression levels of the pluripotency-associated genes octamer-binding transcription factor 4 and Nanog homeobox. These data indicate that radiation-induced CSCs emerge due to the exposure of cells to fractionated irradiation. In addition, the consequent increase in the expression of NED markers is possibly induced by the increased expression of pluripotency-associated genes. Therefore, it can be suggested that cancer cells acquire RR due to increased expression of pluripotency-associated genes following exposure to fractionated irradiation.

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Section: Introductionmentioning

confidence: 99%

Understanding the mechanism underlying the acquisition of radioresistance in human prostate cancer cells

et al. 2019

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“…Radiation tolerance is a major factor related to failure of radiotherapy and poor prognosis for cancer patients. Therefore, radiotherapy resistance has become a major obstacle to overcome [10,11].…”

Section: Discussionmentioning

confidence: 99%

Identification of neoadjuvant radiotherapy resistance genes in rectal cancer using integrated bioinformatics analysis

Liao

Zhang²,

Wang

et al. 2020

Preprint

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The incidence of rectal cancer is increasing year by year. And most patients have been diagnosed in the advanced stages largely because of the special anatomical location of the rectum, resulting in uneasy diagnosis in its early stage. The combination of radiotherapy and chemotherapy is widely accepted as effective treatment to the rectal cancer, significantly reduce the local recurrence rate and improve long-term survival, but the occurrence of radiotherapy resistance of rectal cancer strikingly weaken the responding of treatment. So finding reasons or factors leading to the resistance of neoadjuvant radiotherapy for rectal cancer become very urgent not just for the current clinic but also for development of new therapeutical approaches. To identify potential biomarkers associated with neoadjuvant radiotherapy resistance in rectal cancer using bioinformatics analysis. Firstly, we extracted relevant data from GEO database and analyzed the corresponding data by a series of analytic methods. Then, the candidate genes were identified by performing of the analysis of protein-protein interaction network, KEGG and GO, subsequently comfirmed at the levels of mRNA and Protein with Oncomine and The Human Protein Atlas respectively. Furthermore, these comfirmed genes were submitted to CMap analysis to identify candidate therapeutic compounds for neoadjuvant radiotherapy resistance. We found that the abnormal expression of some chemokines were tightly associated with the rectal cancer neoadjuvant radiotherapy resistance. Especially the upreuglation of Chemokines 9(CXCL9) and Chemokines 10(CXCL10) and downregulation of Chemokines 13(CXCL13) and Chemokines 5(CCL5) might be the potential biomarks of the radiotherapy resistance of rectal cancer. Through a series of analyses, the molecules that may be related to the radiotherapy resistance of rectal cancer were identified that may have a hint effect on the treatment of radiotherapy resistance of rectal cancer.

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“…Radiotherapy is considered as a standard treatment for primary and advanced PCa. However, 20-40% of high-risk PCa patients experience tumor recurrence or distant metastases with one of the causes is radioresistance (3)(4)(5). It has been reported that radioresistance cell reduces the production of reactive oxygen species [ROS; (6)], increases the activation of DNA repair (7), and demonstrates high migratory and invasive abilities (8).…”

Section: Introductionmentioning

confidence: 99%

Identifying Long Non-coding RNA of Prostate Cancer Associated With Radioresponse by Comprehensive Bioinformatics Analysis

Gong

et al. 2020

Front. Oncol.

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Although radiotherapy is greatly successful in the treatment of prostate cancer (PCa), radioresistance is still a major challenge in the treatment. To our knowledge, this study is the first to screen long non-coding RNAs (lncRNAs) associated with radioresponse in PCa by The Cancer Genome Atlas (TCGA). Bioinformatics methods were used to identify the differentially expressed lncRNAs and protein-coding genes (PCGs) between complete response (CR) and non-complete response (non-CR) groups in radiotherapy. Statistical methods were applied to identify the correlation between lncRNAs and radioresponse as well as lncRNAs and PCGs. The correlation between PCGs and radioresponse was analyzed using weighted gene co-expression network analysis (WGCNA). The three online databases were used to predict the potential target miRNAs of lncRNAs and the miRNAs that might regulate PCGs. RT-qPCR was utilized to detect the expression of lncRNAs and PCGs in our PCa patients. A total of 65 differentially expressed lncRNAs and 468 differentially expressed PCGs were found between the two groups of PCa. After the chi-square test, LINC01600 was selected to be highly correlated with radioresponse from the 65 differentially expressed lncRNAs. Pearson correlation analysis found 558 PCGs co-expressed with LINC01600. WGCNA identified the darkred module associated with radioresponse in PCa. After taking the intersection of the darkred module of WGCNA, differentially expressed PCGs between the two groups of PCa, and the PCGs co-expressed with LINC01600, three PCGs, that is, JUND, ZFP36, and ATF3 were identified as the potential target PCGs of LINC01600. More importantly, we detected the expression of LINC01600 and three PCGs using our PCa patients, and finally verified that LINC01600 and JUND were differentially expressed between CR and non-CR groups, excluding ZFP36 and ATF3. Meantime, the potential regulation ability of LINC01600 for JUND in PCa cell lines was initially explored. In addition, we constructed the competing endogenous RNA (ceRNA) network of LINC01600-miRNA-JUND. In conclusion, we initially reveal the association of LINC01600 with radioresponse in PCa and identify its potential target PCGs for further basic and clinical research.

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Radiation induces the generation of cancer stem cells: A novel mechanism for cancer radioresistance

Cited by 83 publications

References 99 publications

Understanding the mechanism underlying the acquisition of radioresistance in human prostate cancer cells

Understanding the mechanism underlying the acquisition of radioresistance in human prostate cancer cells

Identification of neoadjuvant radiotherapy resistance genes in rectal cancer using integrated bioinformatics analysis

Identifying Long Non-coding RNA of Prostate Cancer Associated With Radioresponse by Comprehensive Bioinformatics Analysis

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