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| 1 | DNA Damage, Signaling and Repair: Protecting genomic integrity and reducing the risk of human disease显示文摘DNA is the genetic material that contains the 'instructions' to not only guide the continuation of life but also govern the development, metabolism and functioning of living organisms. DNA damage occurs daily due to various exogenous (environ- | ZHOU PingKun Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China Special Topic Editor | 2011 | Chinese Science Bulletin2011，56，30： | 8 |
| 2 | DNA damage stress induces the dissociation of Smurf1/2 from MDM2 in a slow manner显示文摘The tumor suppressor p53 locates at the key point of cell growth or apoptosis balance, and the expression level of p53 is tightly controlled by ubiquitin ligases including MDM2. Upon DNA damage stresses, p53 was accumulated and activated, leading to cell cycle arrest or apoptosis. We previously showed that Smad ubiquitylation regulatory factor 1/2 (Smurf1/2) promotes p53 degradation by interacting with and stabilizing MDM2, and consequently enhancing MDM2-mediated ubiquitylation of p53. However, it is unclear how the Smurf1-MDM2 interaction is regulated in response to DNA damage stress. Here, we show that in response to etoposide treatment Smurf1 dissociates from MDM2, resulting in MDM2 destabilization and p53 accumulation. The negative regulation of Smurf1 on apoptosis is released. Notably, this dissociation is a slow process rather than a rapid response, implicating high expression of Smurf1 might confer the resistance against p53 activation. Consistent with this notion, we observed that Smurf1/2 ligases are highly expressed in colon cancer, esophageal squamous cell carcinoma and pancreatic cancer tissues, suggesting the oncogenic tendency of Smurf1/2. | NIE Jing LIU Lin ZHAO XiaoHang XIE Ping ZHOU PingKun XING GuiChun LIU XiangJun HE FuChu HAN WeiDong ZHANG LingQiang | 2011 | Chinese Science Bulletin2011，56，30： | 2 |
| 3 | p53-dependent upregulation of PIG3 transcription by γ-ray irradiation and its interaction with KAP1 in responding to DNA damage显示文摘PIG3 (p53-inducible gene 3), originally identified as one of a set of genes induced by p53 before the onset of apoptosis, was assumed to contribute to early cellular response to DNA damage. Here, we studied the relation between p53 status and the increased expression of PIG3 by ionizing radiation (IR), and the related clues regarding the involvement of PIG3 in the cellular response to IR-induced DNA damage signaling. We demonstrated that the pentanucleotide microsatellite sequence was responsible for the p53-dependent induction of PIG3 transcription after irradiation, while sequence upstream of PIG3 promoter could maintain the basal level of expression which was not inducible by irradiation. The interaction of PIG3 and the KRAB-ZFP-associated protein 1 (KAP1), a DNA damage response protein, was revealed. PIG3 nucleus foci were formed 15 min after γ-ray irradiation, and which were found to partially colocalize with the phospho-KAP-1 foci as well as γ-H2AX foci. Although the lac operator tagged EGFP based reporter system revealed that PIG3 does not remodel chromatin in large scale in the cells under normal growing condition, it indeed prompted the chromatin relaxation in the cellular response to DNA damage signaling. All these data suggest that PIG3 is involved in IR-induced DNA damage response, and which maybe partially attribute to its interaction with KAP1. | QIN Xia ZHANG ShiMeng LI Bingi LIU XiaoDan HE XingPeng SHANG ZengFu XU QinZhi ZHAO ZengQiang YE QiNong ZHOU PingKun | 2011 | Chinese Science Bulletin2011，56，30： | 2 |
| 4 | Clustered DNA damage induced by protons radiation in plasmid DNA显示文摘Clustered DNA damage is considered as a critical type of lesions induced by ionizing radiation, which can be converted into the fatal or strong mutagenic complex double strand breaks (DSBs) during damage processing in the cells. The new data show that high energy protons produce more potentially lethal DSBs than low LET radiation. In this study, plasmid DNA were used to in-vestigate and re-evaluate the biological effects induced by the protons with the LET of ~3.6 keV/μm at the molecular level in vitro, including single strand breaks (SSBs), DSBs, isolated and clustered base damages. The results of complex DNA damage detections indicated that protons at the given LET value induce about 1.6 fold more non-DSB clustered DNA damages than the prompt DSB. The DNA damage yields by protons were greater than that by γ-rays, specifically by 6 fold for the isolated type of DNA damage and 14 fold for the clustered damage. Furthermore, the spectrum of damages was also demonstrated to be depended on the radiation quality, with protons producing more DSBs relative to clusters than do γ-rays. | SUI Li WANG Yu WANG Xiao KONG FuQuan LIU JianCheng ZHOU PingKun | 2013 | Chinese Science Bulletin2013，58，26： | 1 |
| 5 | Multi-functions of exonuclease 1 in DNA damage response and cancer susceptibility显示文摘Exonuclease 1(EXO1)can catalyze nucleotide chain excision with its conserved N-terminal domain of 5′ to 3′ exonuclease activity,enabling it to influence diverse biological processes facing the challenges of genotoxic environmental factors such as ionizing radiation.This nuclease activity enables EXO1 to maintain replication forks and telomeres length,to facilitate post-replication DNA repair and to process the end resection step of homologous recombination of DNA double-strand breaks-induced by ionizing radiation.When DNA replication is disrupted or blocked,EXO1 can cleave the broken DNA ends to form 3’ssDNA,leading to repair pathways activation.Excess EXO1-mediated nucleotide excision,however,can introduce an abundance of single-stranded DNA that can cause mutation and recombination via micro-homology-mediated end joining or single-strand annealing mechanisms,contributing to a loss of genetic information.EXO1 activity must therefore be carefully regulated within healthy cells.The mutations and dysregulations of EXO1 can increase the sensitivity of cells to radiation injury and risk of oncogenic transformation,limit the adoption of specific treatments in a range of human diseases.As such,EXO1 represents a promising target for the treatment and prevention of cancer.In the present review,we delineate the structural properties and functional characteristics of EXO1,discuss the relationship between this exonuclease and cancer susceptibility as well as the second cancers related to radiotherapy. | Shuang Yan Shanshan Gao Pingkun Zhou | 2021 | Radiation Medicine and Protection2021，2，4： | 0 |
| 6 | BVAN08 enhances radiosensitivity via downregulation of DNA-PKcs towards hepatic tumor xenograft显示文摘Objective:To study the effects of the novel vanillin derivative BVAN08 on the radiosensitivity of hepatic cancer cells for the purpose of providing evidence for its potential use as a potential radiosensitive drug.Methods:Hepatic cancer Huh-7 cells labeled with luciferase were used to investigate the radiosensitivity induced by BVAN08 in vivo.Colony formation assays and flow cytometry were used to measure the apoptosis and radiosensitivity of Huh-7 cells in vitro produced by BVAN08.Histology and immunohistochemistry were used to evaluate the toxicity of BVAN08 in vivo.Results:BVAN08 induced apoptosis and cell cycle arrest of Huh-7 cells in a time-dependent manner.Moreover,BVAN08 combined with radiation increased the sensitivity of Huh-7 cells toγ-ray radiation and significantly inhibited tumor growth in vivo.The tumor inhibition rates of the BVAN08 treatment group,irradiation treatment group,and combined therapy group were 58%,38%,and 85%,respectively.The DNA-PKcs expression in tumor tissues of the BVAN08 treatment group was lower than that of the control group(P<0.01).BVAN08 inhibited the growth of Huh-7 cells in nude mice bearing tumors,without resulting in any noticeable side effects on bodyweight,livers,hearts,kidneys,or the number of peripheral white blood cells.Conclusions:As a natural food additive derivative,BVAN08 possesses the potential to be used as an effective anticancer drug to increase cell sensitivity to radiotherapy. | Bo Zhang Lantao Liu Sai Hu Zi-Jian Yu Dafei Xie Pingkun Zhou | 2020 | Radiation Medicine and Protection2020，1，3： | 0 |
| 7 | Activation of extracellular signal-regulated kinase by TGF-β1 via TβRⅡ and Smad 7 dependent mechanisms in human bronchial epithelial BEP2D cells显示文摘 | Yanying Huo Yingchun Hu Gang Li Xinrong He Pingkun Zhou Dechang Wu | 2005 | 毒理学杂志2005，19，A03： | 0 |
| 8 | Ubiquitination and degradation of SIK2 by DNA-PKcs deficiency promote radiation-induced mitotic catastrophe显示文摘Salt-inducible kinase 2 (SIK2) is a member of the AMP-activated serine/threonine kinase family. It has been reported that inhibition of SIK2 can enhance the cytotoxicity of paclitaxel,1 promote premitotic apoptosis, and lead to cell cycle arrest in the metaphase.2 Thus, targeting SIK2 may be a therapeutic strategy for cancers drug and radiotherapy resistance. Mitotic catastrophe is a type of abnormal mitosis leading to cell death characterized by the multipolar spindle and multinucleation, which was first discovered during an ionizing radiation (IR)-induced cell damage.3 However, the mechanism of mitotic catastrophe is not well understood. The present study aimed to assess the effect of the knockdown of SIK2 on IR-induced mitotic catastrophe. | Jiaojiao Zhu Ying Zhang Ziyan Yan Jianxiao Wang Ping Wang Xinxin Liang Yuhao Liu Xingkun Ao Maoxiang Zhu Pingkun Zhou Yongqing Gu | 2023 | Genes & Diseases2023，10，2： | 0 |
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