14-3-3σ Contributes to Radioresistance By Regulating DNA Repair and Cell Cycle via PARP1 and CHK2

Chen, Yifan; Li, Zhaomin; Dong, Zizheng; Beebe, Jenny; Yang, Ke; Fu, Liwu; Zhang, Jian-Ting

doi:10.1158/1541-7786.mcr-16-0366

Cited by 30 publications

(25 citation statements)

References 53 publications

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“…Through interaction with the target proteins, 14‐3‐3 proteins including SFN alter the activity, modifications, and intracellular localization of ligands . In particular, SFN regulates DNA repair factors such as DNA‐PKcs, when DNA is damaged by chemotherapy or radiotherapy in human cancer . Based on the previous report, we assume that the high number of gene mutations in Tg‐SPC‐SFN +/− tumors might be due to binding with unknown factor(s), which is associated with the DNA repair system.…”

Section: Discussionmentioning

confidence: 93%

Carcinogen‐induced tumors in SFN‐transgenic mice harbor a characteristic mutation spectrum of human lung adenocarcinoma

et al. 2019

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The landscape of genetic alterations in disease models such as transgenic mice or mice with carcinogen‐induced tumors has provided a huge amount of information that has shed light on the process of tumorigenesis in human non‐small‐cell lung cancer (NSCLC). We have previously identified stratifin (SFN) as a potent oncogene, and generated SFN‐transgenic (Tg‐SPC‐SFN+/−) mice, which express human SFN (hSFN) only in the lung. Here, we have found that carcinogen nicotine‐derived nitrosaminoketone (NNK)‐induced tumors developing in Tg‐SPC‐SFN+/− mice show a similar histology to human lung adenocarcinoma and exhibit high hSFN expression. In order to compare the genetic characteristics of Tg‐SPC‐SFN+/− tumors and human lung adenocarcinoma, the former were subjected to whole‐exome sequencing. Interestingly, Tg‐SPC‐SFN+/− tumors showed the distinct distribution of exonic mutations and high number of mutated genes and transversion. Moreover, Tg‐SPC‐SFN+/− tumors showed 73 genes that were commonly detected in more than 2 tumors, mutations of which were also found in human lung adenocarcinoma. The expression levels of some of these genes were significantly associated with the clinical outcome of lung adenocarcinoma patients. Additionally, mutated genes in Tg‐SPC‐SFN+/− tumors were closely associated with key canonical pathways such as PI3K/AKT signaling and apoptosis signaling. These results suggest that SFN overexpression is a universal abnormality in human lung adenocarcinogenesis and Tg‐SPC‐SFN+/− tumors recapitulate key features of major human lung adenocarcinoma. Therefore, Tg‐SPC‐SFN+/− mice provide a useful model for clarifying the molecular mechanism underlying lung adenocarcinogenesis.

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Section: Discussionmentioning

confidence: 93%

Carcinogen‐induced tumors in SFN‐transgenic mice harbor a characteristic mutation spectrum of human lung adenocarcinoma

et al. 2019

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“… Cell cycle arrest. Following the IR-induced DNA damage detection, molecules in the cell cycle checkpoints can regulate and arrest cell cycle progression, and 14–3-3σ, a member of 14–3-3 protein family, was shown to be closely associated with the radioresistance development by arresting cancer cells in the G2/M phase [ 41 ]. Moreover, tumor cells can utilize two distinct kinase signaling cascades for the DNA damage repair here, including ATM-Chk2 and ATR-Chk1 axes [ 42 ].…”

Section: Introductionmentioning

confidence: 99%

Role of metabolism in cancer cell radioresistance and radiosensitization methods

Tang

Fang

et al. 2018

J Exp Clin Cancer Res

325

214

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BackgroundRadioresistance is a major factor leading to the failure of radiotherapy and poor prognosis in tumor patients. Following the application of radiotherapy, the activity of various metabolic pathways considerably changes, which may result in the development of resistance to radiation.Main bodyHere, we discussed the relationships between radioresistance and mitochondrial and glucose metabolic pathways, aiming to elucidate the interplay between the tumor cell metabolism and radiotherapy resistance. In this review, we additionally summarized the potential therapeutic targets in the metabolic pathways.Short conclusionThe aim of this review was to provide a theoretical basis and relevant references, which may lead to the improvement of the sensitivity of radiotherapy and prolong the survival of cancer patients.

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“…GO and KEGG enrichment analysis results showed that the 558 PCGs co-expressed with LINC01600 were involved in various biological processes such as DNA damage repair, metabolism, cell cycle, and so on. Many studies have shown that DNA damage repair, metabolism, and cell cycle are highly correlated with radiosensitivity (30)(31)(32)(33)(34). This further indicates that LINC01600 and the PCGs co-expressed with it are associated with radioresponse.…”

Section: Discussionmentioning

confidence: 92%

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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14-3-3σ Contributes to Radioresistance By Regulating DNA Repair and Cell Cycle via PARP1 and CHK2

Cited by 30 publications

References 53 publications

Carcinogen‐induced tumors in SFN‐transgenic mice harbor a characteristic mutation spectrum of human lung adenocarcinoma

Carcinogen‐induced tumors in SFN‐transgenic mice harbor a characteristic mutation spectrum of human lung adenocarcinoma

Role of metabolism in cancer cell radioresistance and radiosensitization methods

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

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