截止目前，引用Bioss產品發表的文獻共32641篇，總影響因子160093.22分，發表在Nature, Science, Cell以及Immunity等期刊的文獻共122篇，合作單位覆蓋了清華、北大、復旦、華盛頓大學、麻省理工學院、東京大學以及紐約大學等國際研究機構上百所。
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本文主要分享引用Bioss產品發表文章至Cancer Cell, Molecular Cancer, Advanced Materials, Nature Biomedical Engineering, Bioactive Materials, ACS Nano等期刊的7篇IF＞15的文獻摘要，讓我們一起欣賞吧。
Cancer Cell [IF=48.8]
文獻引用產品：
作者單位：芬蘭赫爾辛基大學
摘要：Anti-tumor immunity is crucial for high-grade serous ovarian cancer(HGSC) prognosis, yet its adaptation upon standard chemotherapy remains poorly understood. Here, we conduct spatial and molecular characterization of 117 HGSC samples collected before and after chemotherapy. Our single-cell and spatial analyses reveal increasingly versatile immune cell states forming spatiotemporally dynamic microcommunities. We describe Myelonets, networks of interconnected myeloid cells that contribute to CD8+ T cell exhaustion post-chemotherapy and show that M1/M2 polarization at the tumor-stroma interface is associated with CD8+ T cell exhaustion and exclusion, correlating with poor chemoresponse. Single-cell and spatial transcriptomics reveal prominent myeloid-T cell interactions via NECTIN2-TIGIT induced by chemotherapy. Targeting these interactions using a functional patient-derived immuno-oncology platform demonstrates that high NECTIN2-TIGIT signaling in matched tumors predicts responses to immune checkpoint blockade. Our discovery of clinically relevant myeloid-driven spatial T cell exhaustion unlocks immunotherapeutic strategies to unleash CD8+ T cell-mediated anti-tumor immunity in HGSC.
Molecular Cancer [IF=27.7]
文獻引用產品：
bs-14542R | eIF3B Rabbit pAb | IHC
bs-51339M | MITF Mouse mAb | WB, IHC
bs-18070R | MHC class I Rabbit pAb | WB
bs-2355R | HLA Class 1 ABC/HLA ABC Rabbit pAb | IHC, IF
bs-22022R | PD-L1 Rabbit pAb | FC
bs-0296P | Mouse IgG | Other作者單位：陸JUN軍醫大學第三附屬醫院
摘要：Programmed cell death protein ligand-1(PD-L1)and major histocompatibility complex I(MHC-I)are key molecules related to tumor immune evasion and resistance to programmed cell death protein 1(PD-1)/PD-L1 blockade. Here, we demonstrated that the upregulation of all miRNAs in the miR-23a/27a/24???2 cluster was correlated with poor survival, immune evasion and PD-1/PD-L1 blockade resistance in patients with non-small cell lung cancer(NSCLC). The overexpression of all miRNAs in the miR-23a/27a/24???2 cluster upregulated PD-L1 expression by targeting Cbl proto-oncogene B(CBLB)and downregulated MHC-I expression by increasing the level of eukaryotic initiation factor 3B(eIF3B)via the targeting of microphthalmia-associated transcription factor(MITF). In addition, we demonstrated that the expression of the miR-23a/27a/24???2 cluster of miRNAs is maintained in NSCLC through increased Wnt/β-catenin signaling-regulated interaction of transcription factor 4(TCF4)and the miR-23a/27a/24???2 cluster promoter. Notably, pharmacologic targeting of the eIF3B pathway dramatically increased sensitivity to PD-1/PD-L1 blockade in patients with high expression of the miR-23a/27a/24???2 cluster in NSCLC. This effect was achieved by increasing MHC-I expression while maintaining high expression of PD-L1 induced by the miR-23a/27a/24???2 cluster. In summary, we elucidate the mechanism by which the miR-23a/27a/24???2 cluster miRNAs maintain their own expression and the molecular mechanism by which the miR-23a/27a/24???2 cluster miRNAs promote tumor immune evasion and PD-1/PD-L1 blockade resistance. In addition, we provide a novel strategy for the treatment of NSCLC expressing high levels of the miR-23a/27a/24???2 cluster.
Advanced Materials [IF=27.4]
文獻引用產品：
AK052 | Cysteine Assay Kit | Other
作者單位：西安電子科技大學
摘要：Cysteine metabolism is a key determinant of the defense against ferroptosis in pancreatic ductal adenocarcinoma(PDAC). Blocking cysteine metabolism may trigger potent ferroptosis in PDAC cells by generating lipid peroxides during tumor metabolic processes. However, current methods to limit cysteine availability fall short, failing to efficiently block cysteine metabolism due to inadequate tumor targeting and compensatory cysteine sources. Inspired by sulfur-metabolizing bacteria, synthetic biology to develop an engineered bacterium capable of directly depleting cysteine to block its metabolism is used. Acting as a living drug, these engineered bacteria colonize the tumor and continuously produce engineered cyst(e)inase enzyme(CGL)under the stimulation of tumor hypoxia. The CGL exhausts the substrate cysteine, completely impeding cysteine metabolism. This process dismantles the ferroptosis defense system in PDAC cells, triggers potent ferroptosis, and achieves efficient treatment. The results demonstrate that engineered bacteria designed for cysteine metabolism modulation possess unparalleled advantages in efficacy, persistence, and precision in blocking cysteine metabolism, making them highly suitable for effective ferroptosis treatment of PDAC.
Nature Biomedical
Engineering [IF=26.8]
文獻引用產品：
C1004 | EGTA solution(0.5mol/L, pH 8.0, sterile) | Other
bs-0295G-BF647 | Goat Anti-Rabbit IgG H&L, BF647 conjugated | IF
作者單位：中國科學院國家納米科學中心
摘要：The development of prophylactic cancer vaccines typically involves the selection of combinations of tumour-associated antigens, tumour-specific antigens and neoantigens. Here we show that membranes from induced pluripotent stem cells can serve as a tumour-antigen pool, and that a nanoparticle vaccine consisting of self-assembled commercial adjuvants wrapped by such membranes robustly stimulated innate immunity, evaded antigen-specific tolerance and activated B-cell and T-cell responses, which were mediated by epitopes from the abundant number of antigens shared between the membranes of tumour cells and pluripotent stem cells. In mice, the vaccine elicited systemic antitumour memory T-cell and B-cell responses as well as tumour-specific immune responses after a tumour challenge, and inhibited the progression of melanoma, colon cancer, breast cancer and post-operative lung metastases. Harnessing antigens shared by pluripotent stem cell membranes and tumour membranes may facilitate the development of universal cancer vaccines.
Bioactive Materials [IF=18]
文獻引用產品：
BA00208 | Cell Counting Kit-8 | Other
作者單位：南方醫科大學第十附屬醫院
摘要：Plant-derived extracellular vesicles(PEVs)have been regarded as a superior source for nanomedicine and drug delivery systems. Nevertheless, their clinical translation is hindered by the lack of clarity and even contradiction in their biomedical applications. Herein, we conducted a comprehensive compositional analysis of four commonly used PEVs to fully understand their functional lipid contents and assess their potential therapeutic applications. The lipidomic analysis revealed the presence of cytotoxic gingerols and shogaols in ginger-derived EVs(GEVs). Subsequent in vitro and in vivo investigations substantiated the remarkable tumor cell inhibitory and tumor growth suppression efficacy of GEVs. The transcriptomic analysis indicated that GEVs regulate the cell cycle and p53 signaling pathways, thereby inducing cancer cell apoptosis. The supplementary proteomic analysis suggested the potential protein markers in PEV research. These findings highlight the value of multi-omics analyses in elucidating the potential therapeutic effects of PEVs and in advancing the development of PEV-based therapies.
ACS Nano [IF=15.8]
文獻引用產品：
bs-1158P | AGEs | Other作者單位：四川大學華西口腔醫院
摘要：Diabetic osteoporosis, a prevalent chronic complication of diabetes, is marked by reduced bone mass, increased bone fragility, and susceptibility to fractures. A significant cause of this condition is the disruption of osteoblastic homeostasis due to prolonged hyperglycemia, which impedes bone regeneration and remodeling. Despite its prevalence, no effective treatments specifically target diabetic osteoporosis. Recently, small-activating RNA(saRNA)therapy has attracted attention for its targeting capacity, high efficacy, and minimal side effects. However, RNA’s inherent properties, such as structural instability, susceptibility to degradation, and poor penetration, limit its applications. To address these limitations, a gene-activating tetrahedral framework nucleic acid(tFNA)with sirtuin-1(SIRT1)gene activation function is developed, termed Tsa. Tsa exhibits an RNA-protecting effect and can effectively penetrate cell membranes to upregulate SIRT1 gene expression. At the histological level, Tsa treatment alleviates diabetic osteoporosis by increasing bone trabecular density and promoting new bone formation. At the cellular level, it switches macrophage polarization toward the anti-inflammatory M2 phenotype while inhibiting the inflammatory M1 phenotype, creating a favorable bone immune microenvironment for osteoblasts. At the genetic level, Tsa activates SIRT1 expression, which deacetylates Acetyl-p65 to block the NF-κB pathway and restore the osteoimmune environment. Overall, this research demonstrates a nanodrug “Tsa”, capable of activating SIRT1 and modulating the bone immune environment, thereby showcasing its immense potential for diabetic osteoporosis treatment.
ACS Nano [IF=15.8]
文獻引用產品：
bs-0295G-HRP |Goat Anti-Rabbit IgG H&L, HRP conjugated | WB
作者單位：南方醫科大學
摘要：Ferroptosis plays an important role in radiotherapy(RT), and the induction of ferroptosis can effectively sensitize radiotherapy. However, the therapeutic efficiency is always affected by ferroptosis resistance, especially SLC7A11(Solute Carrier Family 7 Member 11)-cystine-cysteine-GSH(glutathione)-GPX4(glutathione peroxidase 4)pathway-mediated resistance. In this study, tumor-microenvironment self-activated high-Z element-containing nanoferroptosis inducers, PEGylated Fe–Bi–SS metal–organic frameworks(FBSP MOFs), were developed to sensitize RT. Unexpectedly, ferroptosis-resistant SLC7A11 would be self-adaptively upregulated, leading to self-responsive ferroptosis resistance. Since the conversion from SLC7A11-transported cystine to cysteine is highly glucose-dependent, glucose oxidase(GOx)was incorporated in the MOFs, causing the depletion of NADPH(nicotinamide adenine dinucleotide phosphate)to terminate the conversion from cystine to cysteine, relieving the self-adaptive ferroptosis resistance. Excitingly, the accumulation of cystine would synergistically lead to disulfide stress and trigger disulfidptosis, making a new contribution to enhance therapeutic efficiency. Moreover, the hydrogen peroxide produced during glucose oxidation could also cascade-react with the Fenton reaction, therefore enhancing ferropotosis. Both in vitro and in vivo results suggested that therapeutic efficiency of ferroptosis-mediated radiosensitization could be enhanced benefiting from synergistic disulfidptosis induction, indicating that disulfidptosis might be an efficient strategy to relieve ferroptosis resistance and enhance RT efficiency.
