CHEMICAL ENGINEERING JOURNAL
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2024
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IF 13.3
Yafeng Liu,Shan Ni,Yue Zhao,Wang Yao,Wenjie Wang,Meng Rong,Huizhou Liu,Liangrong Yang
Extracting uranium from wastewater is highly essential for addressing environmental pollution and sustainable development of nuclear power. However, the design and synthesis of functional adsorbents for selective and rapid uranium adsorption remains extremely challenging. Herein, we report the synthesis of a functionalized hyper-cross-linked polymers (PHCP-Q) via an interfacial and coordination microenvironment synergistic modulation strategy for efficient uranium adsorption. The generated interfacial hydrophilic microenvironment allows the rapid migration of uranyl from the solution to the adsorbent and thus enables fast adsorption kinetics. Meanwhile, the fine-tuned coordination microenvironment within pore space creates the hexa-coordinated nano-pocket structure and thereby enhances the selective recognition of uranyl. Remarkably, PHCP-Q achieves adsorption equilibrium within simply 60 min and shows high saturation U(VI) adsorption uptake of 608.95 mg/g. More importantly, PHCP-Q with the cooperation of binding sites exhibits the highest distribution coefficient by an order of magnitude compared with that of other PHCPs. Besides, PHCP-Q possesses good physicochemical stability and recyclability. This study provides a new insight into the future design of highly effective uranium adsorbents by synergistically modulating interfacial and coordination microenvironment, which can be extended to the extraction of other target ions.
研究领域:
环境科学
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材料科学
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核能工程
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产品关联
DOI
高影响因子
ADVANCED FUNCTIONAL MATERIALS
·
2025
·
IF 19
Xuezhe Liu,Xingan Qiu,Pengren Peng,Qiqi Lv,Meijun Tan,Liangshuai Zhang,Qian Feng,Kaiyong Cai
Implants fail due to aseptic loosening remains a critical challenge in orthopedic surgery. This condition arises from poor early-stage osseointegration caused by the bioinert implant interface. Designing immune-active implant coating to timely create a regenerative osteoimmune microenvironment is a recent approach to promote new bone formation. Here, the transient hyperoxia-generating interface coupled with Mg 2+ delivery is developed for the titanium (Ti) to steer osseointegration. This design achieves strong adhesion (388.5 kPa) of the hydrogel coating, ensuring the interfacial stability. Under hypoxic conditions, the engineered interface mitigates cell death and promotes the shift from pro-inflammatory M1 to regenerative M2 macrophages. This immune transition enhances osteogenesis of mesenchymal stem cells (MSCs) and angiogenesis of human umbilical vein endothelial cells (HUVECs) in vitro. Meanwhile, this modified surface demonstrates superior osseointegration results, with histological evidence showing earlier M2 macrophage existence and coordinated bone-vessel growth around the implants. By regulating natural bone healing phases—transient hyperbaric oxygen signaling synergies with Mg 2 ⁺ release for faster inflammation resolution—this platform creates a self-sustaining regenerative niche without exogenous biologics. The results provide a clinically viable strategy to improve implant integration by modulating the osteoimmune microenvironment.
研究领域:
生物材料学
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免疫学
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组织工程
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骨科学
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再生医学
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纳米医学
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转化医学
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产品关联
DOI
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Yifei Wang,Xiaolong Wang,Wenhao Li,Hanwen Huang,Chenyu Di,Qifeng Yang
Ethnopharmacological relevance Trametes robiniophila Murr (Huaier), a traditional Chinese medicine (TCM), has shown promising effects as a complementary therapy in the treatment of multiple kinds of cancers. Aim of the study This study aimed to systematically evaluate whether Huaier could enhance the antitumor effects of palbociclib, a highly selective CDK4/6 inhibitor. Materials and methods A breast cancer xenograft mouse model was constructed to assess the anticancer effects of Huaier and palbociclib. Transcriptomic analysis was performed to identify the differentially expressed genes and associated pathways. Flow cytometry, immunofluorescence and immunohistochemical staining were then conducted to observe the infiltration of immune cells in the tumor microenvironment (TME). The composition of the gut microbiota was explored through 16S rDNA sequencing, and a pseudosterile mouse model was established to verify the contribution of the gut microbiota to the antitumor effects of Huaier and palbociclib. Results Oral administration of Huaier enhanced the antitumor effects of palbociclib in breast cancer. Transcriptomic analysis of tumor tissues revealed that the differentially expressed genes were related to immune functions. Indeed, the addition of Huaier to palbociclib therapy further increased the ratio of CD8 + /CD3 + T cells and the abundance of GzmB + CD8 + T cells in the TME. Mechanistically, sequencing of 16S rDNA revealed that Huaier reshaped the gut microbiota composition in favor of Akkermansia , which positively modulated antitumor immune responses. The pseudosterile mouse model verified the necessity of the gut microbiota for the synergistic effect of Huaier on palbociclib. Furthermore, butyrate, a metabolite of Akkermansia , synergized with palbociclib to suppress tumor progression and promote the infiltration of CD8 + T cells in the TME. Conclusions Our data suggested that Huaier augmented the antitumor effects of palbociclib by increasing the abundance of Akkermansia in gut microbiota, which contributed to the enhancement of anti-tumor immunity. Consequently, combining palbociclib with Huaier may serve as a promising strategy for the treatment of breast cancer.
研究领域:
肿瘤学
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药理学
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免疫学
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微生物学
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中医学
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转录组学
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产品关联
DOI
PubMed
高影响因子
DRUG DELIVERY
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2018
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IF 3.095
Jincheng Yang,Qingzhi Lv,Wei Wei,Zhengtao Yang,Jiajun Dong,Ruoshi Zhang,Qiming Kan,Zhonggui He,Youjun Xu
The efficacy of traditional chemotherapy often suffers from rapid clearance and off-target toxicity. Drug delivery systems and controlled release are applied to improve the therapeutic efficiencies of small-molecule drugs. In this work, two novel oxidative/reductive (Ox/Re) -sensitive and one non-sensitive Paclitaxel (PTX) prodrugs were synthesized with a maleimide group, which rapidly conjugates with albumin in vivo. Albumin serves as a good vehicle to deliver more prodrug to tumors due to the enhanced permeation and retention (EPR) effect. PTX was then released from the prodrugs in glutathione(GSH)/ reactive oxygen species(ROS)-rich tumor microenvironments. This bioresponsive prodrug strategy demonstrates potent chemotherapeutic efficiency in vivo and may be utilized in clinical cancer therapy.
研究领域:
药物化学
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肿瘤学
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生物医学工程
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DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
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2025
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IF 5.6
Jiashuai Yan,Di Wu,Biwen Zhu,Xiaoqi Guan,Xue Zhang,Yibing Guo,Yuhua Lu
As a highly aggressive solid tumor, pancreatic ductal adenocarcinoma (PDAC) is featured by a conspicuous tumor microenvironment (TME) with abundant extracellular matrix (ECM) deposition, such as collagen and hyaluronic acid (HA). Accompanying with the pathological process, the dense matrix caused stiffen microenvironment, which leads to poor chemotherapy. Therefore, understanding the potential mechanism of mechanical microenvironment on PDAC chemoresistance is of great significance. To this end, 3D printed methacrylated gelatin (GelMA) and hyaluronic acid methacryloyly (HAMA) hydrogel model was fabricated to resemble the mechanical microenvironment of PDAC. The results presented that the PDAC cell lines (MIA-PaCa2 and PANC-1) embedded in the hydrogel were distinctively less sensitive to gemcitabine compared to tissue culture plate (TCP) group. Interestingly, immunofluorescence staining and qRT-PCR assay demonstrated that the NRF2 level was elevated, which further upregulated the downstream effectors, such as SLC7A11 and GPX4. Meanwhile, the GSH concentration and GPX4 activity of hydrogel group were increased, while the lipid peroxidation level was reduced, which indicated that the matrix stiffness microenvironment mediated ferroptosis phenotype. Furthermore, RNA interference experiment elaborated that shNRF2 group showcased significantly enhanced sensitivity to gemcitabine, which demonstrated that the biomimetic microenvironment modulated chemoresistance through ferroptosis. All in all, the 3D printed model may serve as a new platform for illustrating the underlying mechanism of the TME induced chemoresistance, and also proposed a novel therapeutic strategy for PDAC through NRF2 inhibition, which effectively promotes ferroptosis to overcome chemoresistance.
研究领域:
肿瘤学
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细胞生物学
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
Journal of Environmental Sciences
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2025
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IF 6.3
Menghe Lou,Li Xiang,Guo Nie,Xueqing Luo,Renna Li,Feng Bi,Xiaole Weng,Zhongbiao Wu
The removal of carbon monoxide (CO) from sintering flue gases remains a significant challenge in industrial gas purification, requiring efficient catalytic systems. This study explores the use of TiO 2 synthesized under supercritical conditions in copper-based catalysts for low-temperature CO oxidation. Experimental results showed enhanced catalytic activity, with complete CO conversion at 120°C, primarily due to a higher Cu⁺ concentration in the catalyst. Characterization techniques (XPS, EPR, CO-DRIFT) confirmed a substantial increase in the Cu⁺ ratio in Cu/sc-TiO 2 (78%) compared to Cu/TiO 2 (71%) before thermal treatment. Additionally, the Cu/sc-TiO 2 -A catalyst exhibited smaller particle size and better dispersion, which contributed to the elevated Cu⁺ ratio after preheating. Thermal treatment increased the Cu⁺ ratio by 11% in Cu/sc-TiO 2 -A, compared to just 3% in Cu/TiO 2 -A, leading to a final Cu⁺ ratio of 89%, which enhanced catalytic activity. DRIFT and TPSR analyses indicated that the Cu/sc-TiO 2 catalyst generated CO during heat treatment, creating a micro-reduction environment that optimized copper valence states and active sites. This study highlights the potential of continuous hydrothermal flow synthesis for modulating catalyst valence states in industrial applications.
研究领域:
材料科学
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催化化学
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环境工程
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产品关联
DOI
PubMed
高影响因子
ACS Omega
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2024
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IF 3.7
Hao Xu,Ning Ning Guo,Chen Ying Zhu,Lin Yan Ye,Xing Yi Yan,Yong Qin Liu,Ze Yan Zhang,Guangji Zhang,Liaqat Hussain
Diterpenoid tanshinones (DTs) are a bioactive fraction extracted from Salvia miltiorrhiza. High-performance liquid chromatography analysis revealed the presence of four compounds, namely, tanshinone IIA, tanshinone I, cryptotanshinone, and dihydrotanshinone. In this study, we aimed to propose a possible mechanism for the anti-lung cancer effect of DT. To do so, we utilized a lung cancer nude mice model and a lung cancer cell line (PC9) to investigate the effect of DT on lung cancer. We employed immunohistochemistry, enzyme-linked immunosorbent assay, hematoxylin and eosin staining, and immunofluorescence to analyze the pharmacological role of DT in the inhibition of lung cancer growth. The results showed that DT inhibited tumor growth, induced apoptosis in the nude mice model, and reduced inflammatory cell infiltration. Additionally, DT inhibited PC9 lung cancer cells, growth, proliferation, and migration. The mechanism of action of DT involves not only directly inhibiting cell proliferation and migration but also improving the tumor microenvironment. DT significantly increased the expression of important intestinal gap junction proteins, such as zonula occludens 1 (ZO-1) and occludin I. This upregulation contributes to the reinforcement of the intestinal mucosal barrier, thereby reducing the paracellular transport of lipopolysaccharides (LPS) through the intestine. Consequently, the decreased LPS levels lead to the inhibition of NF-κB expression and downregulation of macrophage polarization, as indicated by the decreased expression of CD68. In conclusion, this study has confirmed that DT has anti-lung cancer properties by improving the inflammatory tumor microenvironment via regulating macrophage polarization and inhibiting LPS-associated immune response. These results provide new insights into the mechanism of DT action against lung cancer.
研究领域:
肿瘤学
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药理学
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免疫学
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DOI
PubMed
高影响因子
Scientific Reports
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2025
·Vol. 15
·期 1
·1-12
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IF 3.9
Huang Rongfu,Yao Jianfeng,Liu Lei,Li Hua,Huang Baoshan
This study investigated the role of LRRC42 in tumor development and progression using comprehensive methodologies. Analysis of RNA-seq data from the TCGA database revealed that LRRC42 expression is upregulated in various tumor tissues, including bladder cancer (BLCA), breast cancer (BRCA), cholangiocarcinoma (CHOL), colorectal cancer (COAD), esophageal cancer (ESCA), glioblastoma (GBM), head and neck squamous cell carcinoma (HNSC), liver hepatocellular carcinoma (LIHC), lung adenocarcinoma (LUAD), and skin cutaneous melanoma (SKCM), compared to normal tissues. Conversely, LRRC42 was significantly downregulated in kidney chromophobe (KICH) and thyroid carcinoma (THCA) tissues. Single-cell analysis using the TISCH2 database highlighted high LRRC42 expression levels in specific subpopulations across different cancers. Correlation analyses indicated associations between LRRC42 expression and prognosis in multiple tumors, linking it to poor overall survival in several cancer types. Investigations into LRRC42’s interactions with the tumor immune microenvironment and signaling pathways demonstrated significant correlations with immune cells, epithelial-mesenchymal transition molecules, autophagy-related factors, and pyroptosis-related molecules. Focusing on LRRC42’s potential role in hepatocellular carcinoma (HCC), the study uncovered co-expression relationships with Th2 cells and identified genes enriched in mRNA processing and cell cycle regulation pathways. Functional validation through LRRC42 knockdown experiments revealed its critical involvement in promoting cell proliferation, migration, and invasion in HCC cell lines. Collectively, these findings emphasize LRRC42 as a promising therapeutic target for inhibiting HCC progression and suggest its pivotal role in modulating key cellular processes integral to HCC advancement.
研究领域:
肿瘤学
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分子生物学
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生物信息学
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产品关联
DOI
PubMed
高影响因子
CURRENT CANCER DRUG TARGETS
·
2024
·Vol. 25
·期 3
·294-305
·
IF 2.3
Yiping Zheng,Jianfeng Cai,Qiuhong Ji,Luanmei Liu,Kaijun Liao,Lie Dong,Jie Gao,Yinghui Huang
BackgroundLung cancer remains a major global health threat due to its complex microenvironment, particularly the role of neutrophils, which are crucial for tumor development and immune evasion mechanisms. This study aimed to delve into the impact of lung cancer cell-conditioned media on neutrophil functions and their potential implications for lung cancer progression.MethodsEmploying in vitro experimental models, this study has analyzed the effects of lung cancer cell-conditioned media on neutrophil IL-8 and IFN-γ secretion, apoptosis, PD-L1 expression, and T-cell proliferation by using techniques, such as ELISA, flow cytometry, immunofluorescence, and CFSE proliferation assay. The roles of IL-8/PD-L1 in regulating neutrophil functions were further explored using inhibitors for IL-8 and PD-L1.ResultsLung cancer cell lines were found to secrete higher levels of IL-8 compared to normal lung epithelial cells. The conditioned media from lung cancer cells significantly reduced apoptosis in neutrophils, increased PD-L1 expression, and suppressed T-cell proliferation and IFN-γ secretion. These effects were partially reversed in the presence of IL-8 inhibitors in Tumor Tissue Culture Supernatants (TTCS), while being further enhanced by IL-8. Both apoptosis and PD-L1 expression in neutrophils demonstrated dose-dependency to TTCS. Additionally, CFSE proliferation assay results further confirmed the inhibitory effect of lung cancer cell-conditioned media on T-cell proliferation.ConclusionThis study has revealed lung cancer cell-conditioned media to modulate neutrophil functions through regulating factors, such as IL-8, thereby affecting immune regulation and tumor progression in the lung cancer microenvironment.
研究领域:
肿瘤学
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免疫学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
EMBO REPORTS
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2024
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IF 6.5
RenXiaoyu,ShiPeng,SuJing,WeiTonghua,LiJiayi,HuYiping,WuCongying
Tumor metastasis involves cells migrating directionally in response to external chemical signals. Reactive oxygen species (ROS) in the form of H2O2 has been demonstrated as a chemoattractant for neutrophils but its spatial characteristics in tumor microenvironment and potential role in tumor cell dissemination remain unknown. Here we investigate the spatial ROS distribution in 3D tumor spheroids and identify a ROS concentration gradient in spheroid periphery, which projects into a H2O2 gradient in tumor microenvironment. We further reveal the role of H2O2 gradient to induce chemotaxis of tumor cells by activating Src and subsequently inhibiting RhoA. Finally, we observe that the absence of mitochondria cristae remodeling proteins including the mitochondria-localized actin motor Myosin 19 (Myo19) enhances ROS gradient and promotes tumor dissemination. Myo19 downregulation is seen in many tumors, and Myo19 expression is negatively associated with tumor metastasis in vivo. Together, our study reveals the chemoattractant role of tumor microenvironmental ROS and implies the potential impact of mitochondria cristae disorganization on tumor invasion and metastasis.
研究领域:
肿瘤生物学
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细胞生物学
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医学
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产品关联
DOI
PubMed
高影响因子
ACS Nano
·
2023
·
IF 17.1
Chunxiao Gao,Xijun Wang,Bing Yang,Wei Yuan,Wei Huang,Guoju Wu,Jie Ma
Clinical and experimental evidence confirmed bacterial infiltration in a variety of tumors, which is related to the progression and therapeutic effects of the tumors. Although the administration of antibiotics inhibits the growth of bacteria inside the tumor, systemic distribution of antibiotics induces an imbalance of other microbiomes in the body, which in turn leads to the development of new diseases. To address this clinical challenge, we nanonized an antibiotic in this study. Metronidazole, an antibiotic against broad anaerobes, was linked to fluorouridine to form an amphiphilic small molecule, metronidazole–fluorouridine, which further autoassembled as metronidazole–fluorouridine nanoparticles (MTI-FDU) in a hydrophilic solution. The disulfide bond in the linker cleaves in response to high levels of glutathione (GSH) in the tumor microenvironment. The synergistic antitumor effect of MTI-FDU was observed in two animal models of gut cancer with intratumoral bacteria. Analysis revealed that metronidazole delivered by nanoparticles attacked bacteria inside the tumor, while it had minimal effect on gut microbial homeostasis. Further experiments at the cellular and molecular levels disclosed that MTI-FDU shaped the tumor immune microenvironment through clearance of bacteria and bacterial products. In conclusion, we achieved a synergistic antitumor effect by a dual target of both the intratumoral microbiome and tumor cells. Antibiotic-composed nanoparticles have a clinical advantage in the treatment of tumors with bacteria infiltration, which kill pro-tumor bacteria efficiently as well as keep a balanced microbiota of the patient.
研究领域:
肿瘤学
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药理学
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纳米技术
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微生物学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2025
·
IF 5.6
Qianqian Wang,Xin Yuan,Cuijuan Liu,Ying Huang,Lin Li,Yimin Zhu
CAR-T cell therapy has been proven to be effective on hematological tumors, although graft-versus-host disease and cytokine release syndrome(CRS) limit its application to a certain extent. However, CAR-T therapy for solid tumors met challenges, among which the lack of tumor-specific antigens (TSA) and immunosuppressive tumor microenvironment (TME) are the most important factors. CAR-NK could be a good alternative to CAR-T in some ways since they can induce mild CRS and are independent of HLA-matching, but the efficacy of CAR-NKs remains limited in solid tumors. CAR cells armed with multiple tumor targeting molecules may obtain higher therapeutic efficacy against solid tumors. Due to large molecular weight, multivalent scFvs cannot be displayed efficiently on T cells and the high affinity of scFv to the target makes it easy to cause on-target, off-tumor(OTOT) toxicity. Peptides with low molecular weight and slightly lower affinity than scFvs allow immune cells to display multiple peptides to increase killing ability and reduce OTOT toxicity. In our study, peptide-based CAR-NK cells were designed to solve the dilemma of CAR-T in solid tumors. Firstly, the peptide-based CAR-NK92MI cells with A1 peptide were constructed and their inhibitory effects on the growth of A549 tumor cells were identified. Secondly, the tri-specific CAR-NK92MI cells with peptides that simultaneously targeted PD-L1, EGFR and VEGFR2 were developed for the combinatory therapy. Tri-specific CAR-NK92MI exhibited comparable killing activities to scFv-based CAR-NK92MI. Moreover, peptide-based CAR NK92MI mitigated OTOT toxicity. Our study implied that peptide-based CAR-NKs could behave as promising tools in solid tumor
研究领域:
免疫学
·
肿瘤学
·
细胞治疗
✓ 已验证
产品关联
DOI
PubMed
高影响因子