JOURNAL OF ENVIRONMENTAL RADIOACTIVITY
·
2023
·
IF 2.3
Xinchen Chen,Yang Wang,Hongtao Xia,Qi Ren,Yang Li,Lejin Xu,Chuting Xie,Yun Wang
Significant selectivity , reasonable surface modification and increased structural porosity were three key factors to improve the competitiveness of biochar in the adsorption field. In this study, a hydrothermal bamboo-derived biochar modified with phosphate groups (HPBC) was synthesized using “one-can” strategy. BET showed that this method could effectively increase the specific surface area (137.32 m 2 g −1 ) and simulation of wastewater experiments indicated HPBC had an excellent selectivity for U(VI) (70.35%), which was conducive to removal of U(VI) in real and complex environments. The accurate matchings of pseudo-second-order kinetic model , thermodynamic model and Langmuir isotherm showed that at 298 K, pH = 4.0, the adsorption process dominated by chemical complexation and monolayer adsorption was spontaneous, endothermic and disordered. Saturated adsorption capacity of HPBC could reach 781.02 mg g −1 within 2 h. The introduction of phosphoric acid and citric acid by “one-can” method not only provided abundant -PO 4 to assist adsorption, but also activated oxygen-containing groups on the surface of the bamboo matrix. Results showed that adsorption mechanism of U(VI) by HPBC included electrostatic action and chemical complexation involving P–O, P O and ample oxygen-containing functional groups. Therefore, HPBC with high phosphorus content , outstanding adsorption performance, excellent regeneration, remarkable selectivity and green value provided a novel solution for the field of radioactive wastewater treatment.
研究领域:
环境科学
·
材料科学
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产品关联
DOI
PubMed
高影响因子
ACS Omega
·
2023
·
IF 4.1
Yuzhu Li,Kangzhuo Yang,Zhanglan He,Zhipeng Liu,Jialing Lu,Dong Zhao,Jia Zheng,Michael C. Qian
Electronic nose (E-nose) technology is frequently attempted to simulate the human olfactory system to recognize complex odors. Metal oxide semiconductors (MOSs) are E-noses’ most popular sensor materials. However, these sensor responses to different scents were poorly understood. This study investigated the characteristic responses of sensors to volatile compounds in a MOS-based E-nose platform, using baijiu as an evaluation system. The results showed that the sensor array had distinctive responses for different volatile compounds, and the response intensities varied depending on the sensors and the volatile compounds. Some sensors had dose–response relationships in a specific concentration range. Among all the volatiles investigated in this study, fatty acid esters had the greatest contribution to the overall sensor response of baijiu. Different aroma types of Chinese baijiu and different brands of strong aroma-type baijiu were successfully classified using the E-nose. This study provided an understanding of detailed MOS sensor response with volatile compounds, which could be further applied to improve the E-nose technology and its practical application in food and beverages.
研究领域:
食品科学
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分析化学
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DOI
PubMed
高影响因子
CANCER RESEARCH
·
2025
·Vol. 85
·期 20
·3999-4017
·
IF 16.6
Zhao Jian,Zhang Weijie,Zeng Yuanyuan,Lu Di,Ma Chenkang,Zhang Mengzhu,Cai Xin,Huang Zhifan,Yang Hongli,Li Jianjun,Zhu Jianjie,Huang Jian-An,Liu Zeyi
Despite progress in tumor-targeted therapy, oncogenic KRAS remains a major challenge in treating lung adenocarcinoma. In clinical practice, KRAS G12C inhibitors have limited response rates and are associated with acquired drug resistance. Cuproptosis is a recently identified form of copper (Cu)-mediated cell death, and previous studies have revealed that Cu metabolism plays an important role in the development of KRAS-driven tumors. In this study, we revealed the therapeutic value of the Cu ionophore elesclomol (ES) for treating KRAS G12 -mutant–driven lung adenocarcinoma. KRAS G12 -mutant lung adenocarcinoma cells relied on the Cu exporter ATP7A to maintain Cu homeostasis. ES induced cellular Cu accumulation and cuproptosis by upregulating the expression of the E3 ligase OSTM1, which interacted with the IRGY motif of ATP7A to promote ubiquitination and degradation. KRAS G12D transgenic mice and lung cancer organoids derived from the mice were used to validate the therapeutic effects of ES and Cu in vivo and in vitro . These findings indicate that KRAS G12 -driven lung adenocarcinoma relies on ATP7A-mediated Cu metabolic homeostasis, which can be perturbed with ES as an effective treatment strategy. Significance: The copper ionophore elesclomol is effective for treating KRAS-driven lung cancer by activating the OSTM1-ATP7A regulatory axis to perturb copper metabolism homeostasis.
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DOI
PubMed
高影响因子
CANCER RESEARCH
·
2025
·
IF 16.6
Zhang Shijie,Wang Siyu,Wang Yixue,Zhou Tianle,Yang Jiaxin,Xu Jingxue,Li Gen,Zhang Yunyan,Wang Xiaoyuan,Yin Hang
Radioresistance is one of the primary causes of treatment failure in non-small cell lung cancer (NSCLC). In this study, we identified PRMT3 within tumors as a critical mediator impairing both radiotherapy sensitivity and T-cell anti-tumor activity. In tumor cells, PRMT3 mediated arginine methylation of transcription factor TFAP2A, enhancing its binding to the IDO1 promoter. Methylated TFAP2A exhibited a prolonged half life, increased nuclear localization, and enhanced dimer formation, which ultimately led to heightened IDO1 expression that enhanced synthesis of kynurenine (Kyn). The elevated Kyn production boosted radioresistance in tumor cells and suppressed the infiltration and function of CD8+ T cells by activating aryl hydrocarbon receptors (AhR). Interestingly, combined pharmacological inhibition of PRMT3 and IDO1 effectively disrupted the TFAP2A-IDO1-Kyn axis, overcoming radioresistance, activating anti-tumor immunity, and ultimately eradicating tumors. In conclusion, these findings delineate PRMT3-mediated Kyn metabolism as a mechanism of radioresistance and immune evasion in NSCLC, offering valuable insights for potential interventions for treating lung cancer patients.
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PubMed
高影响因子
CANCER RESEARCH
·
2017
·Vol. 77
·期 10
·2735-2745
·
IF 9.122
Fang Min,Li Yongkui,Huang Kai,Qi Shanshan,Zhang Jian,Zgodzinski Witold,Majewski Marek,Wallner Grzegorz,Gozdz Stanislaw,Macek Pawel,Kowalik Artur,Pasiarski Marcin,Grywalska Ewelina,Vatan Linda,Nagarsheth Nisha,Li Wei,Zhao Lili,Kryczek Ilona,Wang Guobin,Wang Zheng,Zou Weiping,Wang Lin
The expression and biological role of IL33 in colon cancer is poorly understood. In this study, we show that IL33 is expressed by vascular endothelial cells and tumor cells in the human colon cancer microenvironment. Administration of human IL33 and overexpression of murine IL33 enhanced human and murine colon cancer cell growth in vivo , respectively. IL33 stimulated cell sphere formation and prevented chemotherapy-induced tumor apoptosis. Mechanistically, IL33 activated core stem cell genes NANOG, NOTCH3 , and OCT3 / 4 via the ST2 signaling pathway, and induced phosphorylation of c-Jun N terminal kinase (JNK) activation and enhanced binding of c-Jun to the promoters of the core stem cell genes. Moreover, IL33 recruited macrophages into the cancer microenvironment and stimulated them to produce prostaglandin E 2 , which supported colon cancer stemness and tumor growth. Clinically, tumor IL33 expression associated with poor survival in patients with metastatic colon cancer. Thus, IL33 dually targets tumor cells and macrophages and endows stem-like qualities to colon cancer cells to promote carcinogenesis. Collectively, our work reveals an immune-associated mechanism that extrinsically confers cancer cell stemness properties. Targeting the IL33 signaling pathway may offer an opportunity to treat patients with metastatic cancer. Cancer Res; 77(10); 2735–45. ©2017 AACR .
研究领域:
肿瘤学
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免疫学
·
分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
CANCER RESEARCH
·
2022
·Vol. 82
·期 19
·3573-3587
·
IF 13.312
Li Yongxu,Wang Tiepeng,Wan Quan,Wang Qing,Chen Zhenzhong,Gao Yuan,Ye Yuchen,Lin Jiusheng,Zhao Bihuan,Wang Huaile,Yang Jinming,Zhao Kai,Lu Na
Glioblastoma (GBM) is the most common type of primary adult brain tumor. Glioma stem cell (GSC) residence and temozolomide (TMZ) resistance in GBM both contribute to poor patient outcome. TRAF4 is a scaffold protein with E3 ubiquitin ligase activity that has recently been discovered to promote invasion and metastasis in several malignancies, but the effects and functions of TRAF4 in GBM remain to be determined. Here, we report that TRAF4 is preferentially overexpressed in GSCs and is required for stem-like properties as well as TMZ sensitivity in GBM cells. TRAF4 specifically interacted with the N-terminal tail of Caveolin-1 (CAV1), an important contributor to the tumorigenicity of GBM cells. TRAF4 regulated CAV1 stability by preventing ZNRF1-mediated ubiquitination and facilitating USP7-mediated deubiquitination independently of its E3 ubiquitin ligase catalytic activity. TRAF4-mediated stabilization of CAV1 activated protumorigenic AKT/ERK1/2 signaling, and disruption of this axis resulted in defects in stemness maintenance. In addition, expression of TRAF4 and CAV1 was positively correlated and predicted poor prognosis in human GBM samples. Screening of common nervous system drugs identified risperidone interaction with TRAF4, and risperidone treatment resulted in the dissociation of TRAF4 and CAV1. Importantly, pharmacologic inhibition of TRAF4 with risperidone potently inhibited self-renewal, abrogated tumorigenicity, and reversed TMZ resistance in GBM. Overall, TRAF4-mediated stabilization of CAV1 promotes stemness and TMZ resistance in GBM, providing a therapeutic strategy that could improve patient outcomes. Significance: The identification of a TRAF4/Caveolin-1 axis that plays a crucial role in malignant progression of glioblastoma provides new insights into the function of TRAF4 in ubiquitin signaling and suggests TRAF4 as a potential therapeutic target.
研究领域:
肿瘤学
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神经科学
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分子生物学
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DOI
PubMed
高影响因子
CANCER RESEARCH
·
2024
·
IF 12.5
Fang Liang,Zhang Li,Wang Mengran,He Yuhao,Yang Jiao,Huang Zengjin,Tan Ying,Fang Ke,Li Jun,Sun Zhiyuan,Li Yanping,Tang Yisen,Liang Weizheng,Cui Huanhuan,Zhu Qionghua,Wu Zhe,Li Yiming,Hu Yuhui,Chen Wei
Epithelial-mesenchymal transition (EMT) is a fundamental cellular process frequently hijacked by cancer cells to promote tumor progression, especially metastasis. EMT is orchestrated by a complex molecular network acting at different layers of gene regulation. In addition to transcriptional regulation, post-transcriptional mechanisms may also play a role in EMT. Here, we performed a pooled CRISPR screen analyzing the influence of 1547 RNA binding proteins (RBPs) on cell motility in colon cancer cells and identified multiple core components of P-bodies (PBs) as negative modulators of cancer cell migration. Further experiments demonstrated that PB depletion by silencing DDX6 or EDC4 could activate hallmarks of EMT thereby enhancing cell migration in vitro as well as metastasis formation in vivo. Integrative multi-omics analysis revealed that PBs could repress the translation of the EMT-driver gene HMGA2, which contributed to PB-meditated regulation of EMT. This mechanism is conserved in other cancer types. Furthermore, endoplasmic reticulum (ER) stress was an intrinsic signal that induced PB disassembly and translational derepression of HMGA2. Taken together, this study has identified a function of PBs in regulation of EMT in cancer.
研究领域:
癌症生物学
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分子生物学
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细胞生物学
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遗传学
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DOI
PubMed
高影响因子
CANCER RESEARCH
·
2026
·
IF 16.6
Liao Fangli,Tong Yanran,Sun Hua,Chen Sen,Wen Siyang,Du Yan-e,Jiang Linshan,Huang Tong,Liu Manran,Chen Weixian,Yang Liping
The immunosuppressive tumor microenvironment (TME) enables cancer cells to evade clinical immunotherapies. Neural networks are vital components of the TME, and interactions between cancer cells, neuronal cells, and immune cells mediate immunosuppression. Hence, understanding the mechanisms of intercellular crosstalk could inform immunomodulatory approaches to enhance immunotherapy efficacy. Here, we found that the vagus nerve regulated the crosstalk between gastric cancer (GC) cells and group 3 innate lymphoid cells (ILC3s), boosting immune resistance in GC by enhancing programmed death ligand 1 (PD-L1) expression. Specifically, the infiltrated vagus nerve released acetylcholine (ACh) that elevated the expression of lipase ABHD16A in GC cells, facilitating the production and secretion of the metabolite lysophosphatidylserine (LysoPS) into the TME. LysoPS facilitated the proliferation and activation of ILC3s in TME, resulting in production of the cytokine interleukin (IL)-22 via the GPR34/AKT/STAT3 axis. In turn, IL-22 triggered the unfolded protein response (UPR) in GC cells, which led to an increase in PD-L1 expression that enhanced immune resistance. Importantly, targeting ACh or the crosstalk between GC cells and ILC3s significantly enhanced the efficacy of anti-PD-L1 immunotherapy. Serum levels of LysoPS and IL-22 were elevated in GC patients, particularly those with perineural invasion. Collectively, these findings provide valuable insights into the crosstalk between GC cells, nerve cells, and ILC3s that regulates immunosuppression and response to ant-PD-L1 immunotherapy, emphasizing the potential clinical significance of this axis for detecting and treating GC.
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DOI
PubMed
高影响因子
CANCER RESEARCH
·
2024
·
IF 12.5
Qiang Yulong,Fan Jiachen,Xie Chuanshuai,Yan Leilei,Song Xiaofei,Zhang Nan,Lin Yan,xiong jie,Zhang Wei,Liu Yu,Wei Lei,Li Yu,Chen Shizhen,Liang Kaiwei,Li Feng
The BET family member BRD4 is a bromodomain-containing protein that plays a vital role in driving oncogene expression. Given their pivotal role in regulating oncogenic networks in various cancer types, BET inhibitors (BETis) have been developed, but the clinical application has been impeded by dose-limiting toxicity and resistance. Understanding the mechanisms of BRD4 activity and identifying predictive biomarkers could facilitate the successful clinical use of BETis. Herein, we showed that KDM5C and BRD4 cooperate to sustain tumor cell growth. Mechanistically, KDM5C interacted with BRD4 and stimulated BRD4 enhancer recruitment. Moreover, binding of the BRD4 C-terminus to KDM5C stimulated the H3K4 demethylase activity of KDM5C. The abundance of both KDM5C-associated BRD4 and H3K4me1/3 determined the transcriptional activation of many oncogenes. Notably, depletion or pharmacological degradation of KDM5C dramatically reduced BRD4 chromatin enrichment and significantly increased BETi efficacy across multiple cancer types in both tumor cell lines and patient-derived organoid models. Furthermore, targeting KDM5C in combination with BETi suppressed tumor growth in vivo in a xenograft mouse model. Collectively, this work reveals a KDM5C-mediated mechanism by which BRD4 regulates transcription, providing a rationale for incorporating BETi into combination therapies with KDM5C inhibitors to enhance treatment efficacy.
研究领域:
肿瘤学
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分子生物学
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癌症研究
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表观遗传学
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DOI
PubMed
高影响因子
CANCER RESEARCH
·
2025
·
IF 16.6
Shang Yan,Li Shuaihu,Xu Tian,Sun Yihua,Li Fei
The CRISPR/Cas9 lentiviral system has emerged as a powerful tool for gene knockout in cancer immunology research. However, the persistent expression of exogenous elements, such as Cas9 and resistance markers, often triggers excessive tumor immune rejection. This can lead to prolonged experimental timelines, increased data variability, biased outcomes, and even experimental failures. To address this challenge, several strategies have been investigated that offer partial solutions, but they have failed so far to comprehensively resolve the issue. In response, we developed the VL-AdCre system, a strategy that enables efficient excision of exogenous expression elements following gene knockout. The VL-AdCre system effectively reduced tumor immune rejection in allograft models, streamlined experimental workflows, and improved the reliability of research outcomes. Overall, this optimized CRISPR/Cas9 lentiviral gene knockout system offers a robust and practical solution for studying gene functions in vivo and advancing immunotherapeutic strategies.
研究领域:
免疫学
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肿瘤学
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分子生物学
·
基因编辑
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转化医学
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产品关联
DOI
PubMed
高影响因子
CANCER RESEARCH
·
2025
·
IF 16.6
Zhou Hai-Meng,Liu Yi,Shi Feng,Qiu Hao-Wen,Li Le,Shu Qi-Peng,Liu Yu-Ying,Wang Bai-Qi,Gao Meng,Du Run-Lei,Ke Shao-Bo,Zhang Xiao-Dong
Ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation, plays a crucial role in colorectal cancer (CRC) progression and therapeutic response. The NRF2 pathway is one of the critical axes in ferroptosis regulation, which governs oxidative stress resistance and iron homeostasis through its downstream targets, including HMOX1, SLC7A11, and others. However, HMOX1 and SLC7A11 exhibit contrasting roles in ferroptosis, with HMOX1 promoting ferroptosis via iron accumulation and lipid peroxidation, while SLC7A11 inhibits ferroptosis by enhancing antioxidant defenses. Here, we identified CLK2 as a key regulator of the delicate balance of the opposing effects of HMOX1 and SLC7A11. CLK2 stabilized KEAP1 to suppress NRF2 activity, resulting in the downregulation of HMOX1 and SLC7A11. Simultaneously, CLK2 downregulated p53, thereby relieving p53-mediated repression of SLC7A11. The dual regulation by CLK2 disrupted the balance between HMOX1 and SLC7A11, leading to excessive activation of HMOX1 in the absence of CLK2, ultimately sensitizing CRC cells to ferroptosis. Additionally, CLK2 promoted CRC proliferation and tumorigenesis in patient-derived organoids, cell lines, and mouse models. Furthermore, combining the ferroptosis inducer Erastin with Oxaliplatin significantly enhanced anti-tumor efficacy in CLK2-deficient xenograft models. Together, this study establishes CLK2 as a critical inhibitor of ferroptosis via the KEAP1/NRF2/HMOX1 and p53/SLC7A11 axes, supporting its potential as a therapeutic target for CRC.
研究领域:
癌症生物学
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分子生物学
·
细胞死亡
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信号转导
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肿瘤学
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药理学
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产品关联
DOI
PubMed
高影响因子
CANCER RESEARCH
·
2025
·
IF 16.6
Ding Wen,Zhu Jianzheng,Mo Jianshan,Ouyang Shumin,Liu Guopin,Su Yingxue,Sun Danyuan,Ye Jiangling,Wu Yanle,Yan Jiayu,Xue Menghan,Yue Peibin,Lu Jin-jian,Wang Libin,Wang Yandong,Zhang Xiaolei
Small cell lung cancer (SCLC) is a highly aggressive malignancy with limited therapeutic options. Neuroendocrine differentiation is a prominent feature of SCLC. This study identified VGF, a secreted neuropeptide precursor, as a critical regulator of neuroendocrine differentiation in SCLC, particularly the ASCL1+ subtype. VGF orchestrated upregulation of the transcription factor ASCL1 through a CREB-dependent mechanism, thereby promoting neuroendocrine differentiation. Furthermore, VGF mediated the transformation of fibroblasts into cancer-associated fibroblasts (CAFs), establishing metabolic coupling between SCLC cells and CAFs via lactate exchange. A therapeutic strategy targeting VGF and monocarboxylate transporter 1 (MCT-1) disrupted neuroendocrine differentiation and SCLC-CAF metabolic coupling, demonstrating significant efficacy in both in vitro and in vivo models. Together, this study provides insights into the mechanisms underlying SCLC neuroendocrine differentiation and reveals targets and therapeutic strategies for advanced SCLC.
研究领域:
癌症生物学
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分子生物学
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神经生物学
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细胞信号传导
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肿瘤微环境
·
代谢调控
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）