摘要:
<jats:sec>
<jats:title>Abstract:</jats:title>
<jats:p>Ginsenoside is the principal active ingredient in ginseng. Several investigations have
found that ginsenosides have anti-inflammatory, antioxidant, anti-apoptotic, anti-cancer, and antiallergic
activities. Ferroptosis is an iron-dependent, non-apoptotic form of cell-regulated death
caused by lipid peroxidation. Iron, lipid, and amino acid metabolism orchestrate the complex ferroptosis
response through direct or indirect regulation of iron accumulation or lipid peroxidation. More
and more research has demonstrated that ginsenoside impacts illnesses via ferroptosis, implying that
ferroptosis might be employed as a novel target of ginsenoside for disease therapy. This article examines
the molecular mechanism of ferroptosis as well as the current advancement of ginsenoside in
influencing disorders via ferroptosis.</jats:p>
</jats:sec>
作者机构:
[Wang, Haohua; Zhang, Jingwen; Peng, Jian] Hainan Univ, Sch Math & Stat, Haikou 570228, Hainan, Peoples R China.;[Wang, Yan] Univ South China, Affiliated Hosp 1, Dept Neurol, Hengyang 421001, Peoples R China.;[Zhang, Jingwen] Hainan Univ, Sch Cyberspace Secur, Haikou 570228, Hainan, Peoples R China.;[Wang, Haohua; Zhang, Jingwen] Hainan Univ, Key Lab Engn Modeling & Stat Computat Hainan Prov, Haikou 570228, Peoples R China.
通讯机构:
[Wang, HH ] H;Hainan Univ, Sch Math & Stat, Haikou 570228, Hainan, Peoples R China.
关键词:
HBV model;Information intervention;Stochastic analysis;Stationary distribution;Optimal control
摘要:
The stochastic fluctuation of information induces the dynamic behavior and disease control strategy to change in the HBV epidemic model, but how stochastic information dissemination affects them is vague. Here, we consider an HBV epidemic model with stochastic information intervention. Using the Lyapunov function, we demonstrate that the system has a unique global positive solution, in addition, we also derive the threshold dynamics to obtain sufficient conditions that can ensure the extinction and persistence, as well as stationarity of the system. Moreover, we qualify the impact of stochasticity of the information on the optimal control strategy of the HBV, indicating that while information intervention could effectively reduce the disease peak, the fluctuation will attenuate this effect, i.e., the stable information is better than the noisy one. Finally, various stochastic and optimal control simulations are performed to verify the theoretical results and verify that optimal control can accelerate the extinction of the disease.
作者机构:
[Wang, Haohua; Liu, Jingchen] Hainan Univ, Sch Math & Stat, Haikou 570228, Hainan, Peoples R China.;[Wang, Yan] Univ South China, Affiliated Hosp 1, Dept Neurol, Hengyang 421001, Hunan, Peoples R China.;[Men, Jiali] Hainan Univ, Sch Life Sci, Haikou 570228, Hainan, Peoples R China.;[Wang, Haohua; Liu, Jingchen] Hainan Univ, Key Lab Engn Modeling & Stat Computat Hainan Prov, Haikou 570228, Hainan, Peoples R China.;[Liu, Jingchen] Shandong Univ, Sch Math, Jinan 250100, Shandong, Peoples R China.
通讯机构:
[Wang, HH ] H;Hainan Univ, Sch Math & Stat, Haikou 570228, Hainan, Peoples R China.;Hainan Univ, Key Lab Engn Modeling & Stat Computat Hainan Prov, Haikou 570228, Hainan, Peoples R China.
关键词:
Network entropy;Gene regulatory network;K2 algorithm;Partial least squares;Network simulation;Time series plateau interval
摘要:
The progress of the cell cycle of yeast involves the regulatory relationships between genes and the interactions proteins. However, it is still obscure which type of protein plays a decisive role in regulation and how to identify the vital nodes in the regulatory network. To elucidate the sensitive node or gene in the progression of yeast, here, we select 8 crucial regulatory factors from the yeast cell cycle to decipher a specific network and propose a simple mixed K2 algorithm to identify effectively the sensitive nodes and genes in the evolution of yeast. Considering the multivariate of cell cycle data, we first utilize the K2 algorithm limited to the stationary interval for the time series segmentation to measure the scores for refining the specific network. After that, we employ the network entropy to effectively screen the obtained specific network, and simulate the gene expression data by a normal distribution approximation and the screened specific network by the partial least squares method. We can conclude that the robustness of the specific network screened by network entropy is better than that of the specific network with the determined relationship by comparing the obtained specific network with the determined relationship. Finally, we can determine that the node CDH1 has the highest score in the specific network through a sensitivity score calculated by network entropy implying the gene CDH1 is the most sensitive regulatory factor. It is clearly of great potential value to reconstruct and visualize gene regulatory networks according to gene databases for life activities. Here, we present an available algorithm to achieve the network reconstruction by measuring the network entropy and identifying the vital nodes in the specific nodes. The results indicate that inhibiting or enhancing the expression of CDH1 can maximize the inhibition or enhancement of the yeast cell cycle. Although our algorithm is simple, it is also the first step in deciphering the profound mystery of gene regulation.
期刊:
Journal of Biological Chemistry,2024年300(3):105721 ISSN:0021-9258
通讯作者:
Wang, Yugang
作者机构:
[Zeng, Xiao; Zhou, Runxin; Wang, Yu; Tong, Fuqiang; Guo, Dingyuan; Yin, Sibi; Wang, Yugang] Department of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China;[Yu, Weixing] Department of Biochemistry and Molecular Biology, College of Basic Medicine, Jining Medical University, Jining, 272067, China;[Jiang, Li] Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China, 430060;[Jiang, Li] Department of Neurology, The Affiliated Nanhua Hospital, University of South China, Hengyang, 421001, China;[He, Leya] Department of Gastrointestinal Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China
通讯机构:
[Yugang Wang] D;Department of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China<&wdkj&>Cell Architecture Research Center, Huazhong University of Science and Technology, Wuhan, Hubei, China
摘要:
ATP-binding cassette protein A1 (ABCA1) is a key protein in the transport of intracellular cholesterol to the extracellular and plays an important role in reduc-ing cholesterol accumulation in surrounding tissues. Bibliometric analysis refers to the cross-science of quan-titative analysis of a variety of documents by mathemati-cal and statistical methods. It combines an analysis of structural and temporal patterns in scholarly publica-tions with a description of topic concentration and types of uncertainty. This paper analyzes the history, hotspot, and development trend of ABCA1 through bibliometrics. It will provide readers with the research status and development trend of ABCA1 and help the hot research in this field explore new research directions. After screening, the research on ABCA1 is still in a hot phase in the past 20 years. ABCA1 is emerging in previously unrelated disciplines such as cancer. There were 551 key-words and 6888 breakout citations counted by CiteSpace. The relationship between cancer and cardiovascular dis-ease has been linked by ABCA1. This review will guide readers who are not familiar with ABCA1 research to quickly understand the development process of ABCA1 and provide researchers with a possible future research focus on ABCA1. (Curr Probl Cardiol 2024;49:102036.)
摘要:
Atherosclerosis is a chronic inflammatory disease of the arterial wall caused by an imbalance of lipid metabolism and a maladaptive inflammatory response. A variety of harmful cellular changes associated with atherosclerosis include endothelial dysfunction, the migration of circulating inflammatory cells to the arterial wall, the production of proinflammatory cytokines, lipid buildup in the intima, local inflammatory responses in blood vessels, atherosclerosis-associated apoptosis, and autophagy. PTEN inhibits the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/AKT)/mammalian target of rapamycin (mTOR) pathway through its lipid phosphatase activity. Previous studies have shown that PTEN is closely related to atherosclerosis. This article reviews the role of PTEN in atherosclerosis from the perspectives of autophagy, apoptosis, inflammation, proliferation, and angiogenesis.
摘要:
Neuronal ferroptosis plays a critical role in the pathogenesis of cognitive deficits. The present study explored whether artemisinin protected type 2 diabetes mellitus (T2DM) mice from cognitive impairments by attenuating neuronal ferroptosis in the hippocampal CA1 region. STZ-induced T2DM mice were treated with artemisinin (40 mg/kg, i.p.), or cotreated with artemisinin and Nrf2 inhibitor MEL385 or ferroptosis inducer erastin for 4 weeks. Cognitive performance was determined by the Morris water maze and Y maze tests. Hippocampal ROS, MDA, GSH, and Fe2+ contents were detected by assay kits. Nrf2, p-Nrf2, HO-1, and GPX4 proteins in hippocampal CA1 were assessed by Western blotting. Hippocampal neuron injury and mitochondrial morphology were observed using H&E staining and a transmission electron microscope, respectively. Artemisinin reversed diabetic cognitive impairments, decreased the concentrations of ROS, MDA and Fe2+, and increased the levels of p-Nr2, HO-1, GPX4 and GSH. Moreover, artemisinin alleviated neuronal loss and ferroptosis in the hippocampal CA1 region. However, these neuroprotective effects of artemisinin were abolished by Nrf2 inhibitor ML385 and ferroptosis inducer erastin. Artemisinin effectively ameliorates neuropathological changes and learning and memory decline in T2DM mice; the underlying mechanism involves the activation of Nrf2 to inhibit neuronal ferroptosis in the hippocampus.
摘要:
BACKGROUND: Social isolation not only increases the risk of mortality in later life but also causes depressive symptoms, cognitive and physical disabilities. Although RNA m6A modifications are suggested to play key roles in brain development, neuronal signaling and neurological disorders, both the roles of m6A and the enzymes that regulate RNA m6A modification in social isolation induced abnormal behavior is unknown. The present study aims to explore the possible epitranscriptomic role of RNA m6A modifications and its enzymes in social isolation induced impaired behavior. METHODS: 3-4weeks mice experiencing 8weeks social isolation stress (SI) were used in the present study. We quantified m6A levels in brain regions related to mood and cognitive behavior. And the expression of hippocampal m6A enzymes was also determined. The role of hippocampal m6A and its enzymes in SI induced abnormal behavior was further verified by the virus tool. RESULTS: SI led to not only depressive and anxiety-like behaviors but also cognitive impairment, with corresponding decreases in hippocampal m6A and METTL14. Hippocampal over-expression METTL14 with lentivirus not only rescued these behaviors but also enhanced the hippocampal m6A level. Hippocampal over-expression METTL14 resulted in increased synaptic related genes. CONCLUSIONS: We provide the first evidence that post-weaning social isolation reduces hippocampal m6A level and causes altered expression of m6A enzyme in mice. Importantly, hippocampal METTL14 over-expression alleviated the SI-induced depression/anxiety-like and impaired cognitive behaviors and enhanced m6A level and synaptic related genes expression.
期刊:
Journal of the European Academy of Dermatology and Venereology,2024年38(8):1478-1490 ISSN:0926-9959
通讯作者:
Zhao, FJ;Liu, SQ
作者机构:
[Xiong, Shun; Zhao, Feijun; Liu, Shuangquan; Liu, Zhaoping; Ding, Xuan; Huang, Shaobin; Yao, Jiangchen; Zhang, Xiaohong; Xu, Man] Univ South China, Hengyang Med Coll, Inst Pathogen Biol, Hengyang, Peoples R China.;[Xiong, Shun; Zhao, Feijun; Liu, Shuangquan; Liu, Zhaoping; Ding, Xuan; Huang, Shaobin; Yao, Jiangchen; Zhang, Xiaohong; Xu, Man] Univ South China, Hengyang Med Coll, Key Lab Special Pathogen Prevent & Control Hunan P, Hengyang, Peoples R China.;[Xiong, Shun; Zhao, Feijun; Liu, Shuangquan; Liu, Zhaoping; Ding, Xuan; Huang, Shaobin; Yao, Jiangchen; Zhang, Xiaohong; Xu, Man] Univ South China, Affiliated Hosp 1, Hengyang Med Coll, Dept Clin Lab Med, Hengyang, Peoples R China.;[Zhao, Feijun; Zhao, FJ] Univ South China, Hengyang Med Coll, Inst Pathogen Biol, Hengyang 421001, Peoples R China.;[Zhao, Feijun; Zhao, FJ] Univ South China, Hengyang Med Coll, Key Lab Special Pathogen Prevent & Control Hunan P, Hengyang 421001, Peoples R China.
通讯机构:
[Zhao, FJ ; Liu, SQ ] U;Univ South China, Hengyang Med Coll, Inst Pathogen Biol, Hengyang 421001, Peoples R China.;Univ South China, Hengyang Med Coll, Key Lab Special Pathogen Prevent & Control Hunan P, Hengyang 421001, Peoples R China.;Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Inst Microbiol & Infect Dis,Dept Clin Lab Med, Hengyang 421001, Peoples R China.
摘要:
<jats:title>Abstract</jats:title><jats:p><jats:italic>Treponema pallidum</jats:italic> is the causative factor of syphilis, a sexually transmitted disease (STD) characterized by perivascular infiltration of inflammatory cells, vascular leakage, swelling and proliferation of endothelial cells (ECs). The endothelium lining blood and lymphatic vessels is a key barrier separating body fluids from host tissues and is a major target of <jats:italic>T. pallidum</jats:italic>. In this review, we focus on how <jats:italic>T. pallidum</jats:italic> establish intimate interactions with ECs, triggering endothelial dysfunction such as endothelial inflammation, abnormal repairment and damage of ECs. In addition, we summarize that migration and invasion of <jats:italic>T. pallidum</jats:italic> across vascular ECs may occur through two pathways. These two mechanisms of transendothelial migration are paracellular and cholesterol‐dependent, respectively. Herein, clarifying the relationship between <jats:italic>T. pallidum</jats:italic> and endothelial dysfunction is of great significance to provide novel strategies for diagnosis and prevention of syphilis, and has a great potential prospect of clinical application.</jats:p>
摘要:
Quinic acid (QA) and its derivatives have good lipid-lowering and hepatoprotective functions, but their role in atherosclerosis remains unknown. This study attempted to investigate the mechanism of QA on atherogenesis in Apoe−/− mice induced by HFD. HE staining and oil red O staining were used to observe the pathology. The PCSK9, Mac-3 and SM22a expressions were detected by IHC. Cholesterol, HMGB1, TIMP-1 and CXCL13 levels were measured by biochemical and ELISA. Lipid metabolism and the HMGB1-SREBP2-SR-BI pathway were detected by PCR and WB. 16 S and metabolomics were used to detect gut microbiota and serum metabolites. QA or low-frequency ABX inhibited weight gain and aortic tissue atherogenesis in HFD-induced Apoe−/− mice. QA inhibited the increase of cholesterol, TMA, TMAO, CXCL13, TIMP-1 and HMGB1 levels in peripheral blood of Apoe−/− mice induced by HFD. Meanwhile, QA or low-frequency ABX treatment inhibited the expression of CAV-1, ABCA1, Mac-3 and SM22α, and promoted the expression of SREBP-1 and LXR in the vascular tissues of HFD-induced Apoe−/− mice. QA reduced Streptococcus_danieliae abundance, and promoted Lactobacillus_intestinalis and Ileibacterium_valens abundance in HFD-induced Apoe−/− mice. QA altered serum galactose metabolism, promoted SREBP-2 and LDLR, inhibited IDOL, FMO3 and PCSK9 expression in liver of HFD-induced Apoe−/− mice. The combined treatment of QA and low-frequency ABX regulated microbe-related Glycoursodeoxycholic acid and GLYCOCHENODEOXYCHOLATE metabolism in HFD-induced Apoe−/− mice. QA inhibited TMAO or LDL-induced HCAECs damage and HMGB1/SREBP2 axis dysfunction, which was reversed by HMGB1 overexpression. QA regulated the gut-liver lipid metabolism and chronic vascular inflammation of TMA/TMAO through gut microbiota to inhibit the atherogenesis in Apoe−/− mice, and the mechanism may be related to the HMGB1/SREBP2 pathway.
作者机构:
[Qin, Qin; Zhong, Li-Yuan; Zeng, Xi; Weng, Xin; Cao, De-Liang; Xie, Li-Hua; Ge, Wen-Jun] Univ South China, Canc Res Inst, Hunan Engn Res Ctr Early Diag & Treatment Liver Ca, Hengyang Med Sch,Hunan Prov Key Lab Tumor Cellular, 28 Changsheng West Rd, Hengyang 421001, Hunan, Peoples R China.;[Zeng, Wei-Hong] Hunan Normal Univ, Coll Life Sci, Lab Mol & Stat Genet, Changsha 410081, Hunan, Peoples R China.;[Lai, Zhen] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Pathol, Hengyang 421001, Hunan, Peoples R China.;[Liu, Peng] Hunan Normal Univ, Affiliated Hosp 1, Peoples Hosp, Dept Gastroenterol, Changsha 410005, Hunan, Peoples R China.
通讯机构:
[Zeng, X ] U;Univ South China, Canc Res Inst, Hunan Engn Res Ctr Early Diag & Treatment Liver Ca, Hengyang Med Sch,Hunan Prov Key Lab Tumor Cellular, 28 Changsheng West Rd, Hengyang 421001, Hunan, Peoples R China.
摘要:
Chemotherapy remains a prevalent treatment for a wide range of tumors; however, the majority of patients undergoing conventional chemotherapy experience varying levels of chemoresistance, ultimately leading to suboptimal outcomes. The present article provided an in‑depth review of chemotherapy resistance in tumors, emphasizing the underlying factors contributing to this resistance in tumor cells. It also explored recent advancements in the identification of key molecules and molecular mechanisms within the primary chemoresistant pathways.
摘要:
BACKGROUND: Under normal circumstances, high-density lipoprotein (HDL) is considered to have cardiovascular protective effects, but the impact of oxidized HDL (ox-HDL) on vascular endothelial function remains poorly understood. Mitochondrial function is closely related to endothelial function, and hydrogen sulfide (H₂S) is a gas with endothelial protective properties. The novel hydrogen sulfide donor AP39 can target mitochondria to release H₂S, but the combined effects of ox-HDL and AP39 on vascular endothelium are not well studied. METHODS: We established a cell model of ox-HDL-induced endothelial cell damage and mitochondrial dysfunction using human umbilical vein endothelial cells (HUVECs) and conducted AP39 pretreatment. The experiments confirmed the functional damage and mitochondrial dysfunction in HUVECs caused by ox-HDL. Additionally, to further explore the role of SIRT1 in AS, we analyzed SIRT1 expression in AS carotid artery tissue. This included the analysis of differentially expressed genes from AS-related datasets, presented through volcano plots and heatmaps, with enrichment analysis of downregulated genes in KEGG pathways and GO functions. Furthermore, we evaluated the differences in SIRT1 expression in coronary arteries with varying degrees of stenosis and in early and late-stage AS carotid artery tissues, and analyzed data from SIRT1 knockout mouse models. RESULTS: The experimental results indicate that AP39 effectively alleviated ox-HDL-induced endothelial cell damage and mitochondrial dysfunction by upregulating SIRT1 expression. MTT and CCK-8 assays showed that ox-HDL treatment led to decreased cell viability and proliferation in HUVECs, reduced eNOS expression, and significantly increased levels of ICAM-1, IL-6, and TNF-α, along with enhanced monocyte adhesion. These findings reveal the damaging effects of ox-HDL on HUVECs. Transcriptomic data indicated that while SIRT1 expression did not significantly differ in coronary arteries with varying degrees of stenosis, it was notably downregulated in AS carotid artery tissues, especially in late-stage AS tissues. KEGG pathway enrichment analysis revealed that SIRT1 downregulated genes were associated with processes such as vascular smooth muscle contraction, while GO analysis showed that these downregulated genes were involved in muscle system processes and muscle contraction functions, further confirming SIRT1's critical role in AS pathology. In transcriptomic data from the SIRT1 knockout mouse model, elevated levels of inflammation-related proteins IL-6 and TNF-α were observed after SIRT1 knockout, along with decreased expression of the chaperone protein PGC-1α. The expression of mitochondrial-related functional proteins Nrf2 and PGC-1α was positively correlated with SIRT1 expression, while inflammation-related proteins ICAM-1, IL-6, IL-20, and TNF-α were negatively correlated with SIRT1 expression. We further discovered that ox-HDL triggered mitochondrial dysfunction, as evidenced by reduced expression of Mfn2, Nrf2, PGC1-α, UCP-1, and SIRT1, corroborating the results from the previous database analysis. Additionally, mitochondrial dysfunction was characterized by decreased mitochondrial membrane potential (MMP), increased mitochondrial ROS levels, and reduced ATP content, further impacting cellular energy metabolism and respiratory function. Subsequent experimental results showed that the addition of AP39 mitigated these adverse effects, as evidenced by decreased levels of ICAM-1, IL-6, and TNF-α, increased eNOS expression, reduced monocyte adhesion, increased mitochondrial H₂S content, and upregulated expression of SIRT1 protein associated with mitochondrial function, reduced ROS levels, and increased ATP content. Furthermore, validation experiments using the SIRT1 inhibitor EX527 confirmed that AP39 alleviated ox-HDL-induced endothelial cell damage and mitochondrial dysfunction by upregulating SIRT1 expression. CONCLUSION: Ox-HDL can induce damage and mitochondrial dysfunction in HUVECs, while AP39 inhibits ox-HDL-induced endothelial cell damage and mitochondrial dysfunction by upregulating SIRT1.
摘要:
BACKGROUND: Depression is a highly prevalent comorbidity arising in patients with Parkinson's disease (PD). However, depression in patients with PD is poorly treated. Hydrogen sulfide (H(2)S), a neuromodulator, has the potential to relieve depression. OBJECTIVE: To investigate whether H(2)S attenuates depression-like behaviours in a rat model of PD and examine the underlying mechanisms. METHODS: We utilised rotenone to develop a PD model with subcutaneous injections in the dorsal cervical region of Sprague-Dawley rats. The depression-like behaviours in the rotenone-induced PD model rats were assessed through forced swimming, tail suspension, open field, novelty-suppressed feeding, and elevated plus-maze tests. The expression of postsynaptic density protein-95 and synapsin-1, related to synaptic plasticity, was detected using Western blot in the hippocampus. The hippocampal ultrastructure, including the synaptic density, length of the synaptic active zone, postsynaptic density thickness, and synaptic gap width, was detected using transmission electron microscopy. RESULTS: We proved that sodium hydrosulfide (NaHS; a donor of H(2)S) significantly attenuated the depression-like behaviours and disorders of hippocampal synaptic plasticity in rotenone-induced PD rats. Furthermore, inhibition of the hippocampal Warburg effect by 2-deoxyglucose abolished NaHS-enhanced hippocampal synaptic plasticity and reversed NaHS-attenuated depression-like behaviours in the rotenone-induced PD rats. CONCLUSION: H(2)S attenuates PD-associated depression by improving the hippocampal synaptic plasticity in a hippocampal Warburg effect-dependent manner.
作者机构:
[Xie, Dafei; Gu, Yongqing; Wang, Ping; Zhu, Jiaojiao; Guan, Hua; Zhou, Lin; Yan, Ziyan; Liu, Yuhao; Gao, Shanshan; Zhou, Ping-Kun] Beijing Key Laboratory for Radiobiology Beijing Institute of Radiation Medicine Beijing China;[Chen, Huixi; Gu, Yongqing; Liang, Xinxin; Zhou, Shenghui; Ao, Xingkun] Hengyang Medical College University of South China Hengyang China;[Hou, Yifan; Gu, Yongqing] College of Life Sciences Hebei University Baoding China
关键词:
DNA‐PKcs;NHEJ;RET/PTC1 rearrangement;low‐dose ionizing radiation;thyroid cancer
摘要:
We found that low‐dose IR can induce RET/PTC1 rearrangement in N‐thy‐ori‐3‐1 cell and there is a dose‐dependent manner between dose and rearrangement rate. We showed that this progress of IR‐induced RET/PTC1 rearrangement requires NHEJ and not HR. Moreover, DNA‐PKcs inhibition decreased the repair efficiency of NHEJ. Importantly, the RET/PTC1 rearrangement induced by IR was significantly decreased by DNA‐PKcs. Abstract Thyroid cancer incidence increases worldwide annually, primarily due to factors such as ionizing radiation (IR), iodine intake, and genetics. Papillary carcinoma of the thyroid (PTC) accounts for about 80% of thyroid cancer cases. RET/PTC1 (coiled‐coil domain containing 6 [CCDC6]‐rearranged during transfection) rearrangement is a distinctive feature in over 70% of thyroid cancers who exposed to low doses of IR in Chernobyl and Hiroshima‒Nagasaki atomic bombings. This study aims to elucidate mechanism between RET/PTC1 rearrangement and IR in PTC. N‐thy‐ori‐3‐1 cells were subjected to varying doses of IR (2/1/0.5/0.2/0.1/0.05 Gy) of IR at different days, and result showed low‐dose IR‐induced RET/PTC1 rearrangement in a dose‐dependent manner. RET/PTC1 has been observed to promote PTC both in vivo and in vitro. To delineate the role of different DNA repair pathways, SCR7, RI‐1, and Olaparib were employed to inhibit non‐homologous end joining (NHEJ), homologous recombination (HR), and microhomology‐mediated end joining (MMEJ), respectively. Notably, inhibiting NHEJ enhanced HR repair efficiency and reduced IR‐induced RET/PTC1 rearrangement. Conversely, inhibiting HR increased NHEJ repair efficiency and subsequent RET/PTC1 rearrangement. The MMEJ did not show a markable role in this progress. Additionally, inhibiting DNA‐dependent protein kinase catalytic subunit (DNA‐PKcs) decreased the efficiency of NHEJ and thus reduced IR‐induced RET/PTC1 rearrangement. To conclude, the data suggest that NHEJ, rather than HR or MMEJ, is the critical cause of IR‐induced RET/PTC1 rearrangement. Targeting DNA‐PKcs to inhibit the NHEJ has emerged as a promising therapeutic strategy for addressing IR‐induced RET/PTC1 rearrangement in PTC.