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学者姓名：阎新龙
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Abstract ：
Over the past decade, organoids have emerged as a prevalent and promising research tool, mirroring the physiological architecture of the human body. However, as the field advances, the traditional use of animal or tumor-derived extracellular matrix (ECM) as scaffolds has become increasingly inadequate. This shift has led to a focus on developing synthetic scaffolds, particularly hydrogels, that more accurately mimic three-dimensional (3D) tissue structures and dynamics in vitro. The ECM-cell interaction is crucial for organoid growth, necessitating hydrogels that meet organoid-specific requirements through modifiable physical and compositional properties. Advanced composite hydrogels have been engineered to more effectively replicate in vivo conditions, offering a more accurate representation of human organs compared to traditional matrices. This review explores the evolution and current uses of decellularized ECM scaffolds, emphasizing the application of decellularized ECM hydrogels in organoid culture. It also explores the fabrication of composite hydrogels and the prospects for their future use in organoid systems.
Keyword ：
Microenvironment Microenvironment Hydrogels Hydrogels Natural-based biomaterials Natural-based biomaterials Decellularized Extracellular Matrix Decellularized Extracellular Matrix Organoid culture Organoid culture
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| GB/T 7714 | Li, Chen , An, Ni , Song, Qingru et al. Enhancing organoid culture: harnessing the potential of decellularized extracellular matrix hydrogels for mimicking microenvironments [J]. | JOURNAL OF BIOMEDICAL SCIENCE , 2024 , 31 (1) . |
| MLA | Li, Chen et al. "Enhancing organoid culture: harnessing the potential of decellularized extracellular matrix hydrogels for mimicking microenvironments" . | JOURNAL OF BIOMEDICAL SCIENCE 31 . 1 (2024) . |
| APA | Li, Chen , An, Ni , Song, Qingru , Hu, Yuelei , Yin, Wenzhen , Wang, Qi et al. Enhancing organoid culture: harnessing the potential of decellularized extracellular matrix hydrogels for mimicking microenvironments . | JOURNAL OF BIOMEDICAL SCIENCE , 2024 , 31 (1) . |
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Abstract ：
Background Traumatic brain injury (TBI) leads to cell and tissue impairment, as well as functional deficits. Stem cells promote structural and functional recovery and thus are considered as a promising therapy for various nerve injuries. Here, we aimed to investigate the role of ectoderm-derived frontal bone mesenchymal stem cells (FbMSCs) in promoting cerebral repair and functional recovery in a murine TBI model. Methods A murine TBI model was established by injuring C57BL/6 N mice with moderate-controlled cortical impact to evaluate the extent of brain damage and behavioral deficits. Ectoderm-derived FbMSCs were isolated from the frontal bone and their characteristics were assessed using multiple differentiation assays, flow cytometry and microarray analysis. Brain repairment and functional recovery were analyzed at different days post-injury with or without FbMSC application. Behavioral tests were performed to assess learning and memory improvements. RNA sequencing analysis, immunofluorescence staining, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to examine inflammation reaction and neural regeneration. In vitro co-culture analysis and quantification of glutamate transportation were carried out to explore the possible mechanism of neurogenesis and functional recovery promoted by FbMSCs. Results Ectoderm-derived FbMSCs showed fibroblast like morphology and osteogenic differentiation capacity. FbMSCs were CD105, CD29 positive and CD45, CD31 negative. Different from mesoderm-derived MSCs, FbMSCs expressed the ectoderm-specific transcription factor Tfap2 beta. TBI mice showed impaired learning and memory deficits. Microglia and astrocyte activation, as well as neural damage, were significantly increased post-injury. FbMSC application ameliorated the behavioral deficits of TBI mice and promoted neural regeneration. RNA sequencing analysis showed that signal pathways related to inflammation decreased, whereas those related to neural activation increased. Immunofluorescence staining and qRT-PCR data revealed that microglial activation and astrocyte polarization to the A1 phenotype were suppressed by FbMSC application. In addition, FGF1 secreted from FbMSCs enhanced glutamate transportation by astrocytes and alleviated the cytotoxic effect of excessive glutamate on neurons. Conclusions Ectoderm-derived FbMSC application significantly alleviated neuroinflammation, brain injury, and excitatory toxicity to neurons, improved cognition and behavioral deficits in TBI mice. Therefore, ectoderm-derived FbMSCs could be ideal therapeutic candidates for TBI which mostly affect cells from the same embryonic origins as FbMSCs.
Keyword ：
Glutamate excitotoxicity Glutamate excitotoxicity Traumatic brain injury Traumatic brain injury Neuroinflammation Neuroinflammation Frontal bone mesenchymal stem cells Frontal bone mesenchymal stem cells
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| GB/T 7714 | Qin, Qiaozhen , Wang, Ting , Xu, Zhenhua et al. Ectoderm-derived frontal bone mesenchymal stem cells promote traumatic brain injury recovery by alleviating neuroinflammation and glutamate excitotoxicity partially via FGF1 [J]. | STEM CELL RESEARCH & THERAPY , 2022 , 13 (1) . |
| MLA | Qin, Qiaozhen et al. "Ectoderm-derived frontal bone mesenchymal stem cells promote traumatic brain injury recovery by alleviating neuroinflammation and glutamate excitotoxicity partially via FGF1" . | STEM CELL RESEARCH & THERAPY 13 . 1 (2022) . |
| APA | Qin, Qiaozhen , Wang, Ting , Xu, Zhenhua , Liu, Shuirong , Zhang, Heyang , Du, Zhangzhen et al. Ectoderm-derived frontal bone mesenchymal stem cells promote traumatic brain injury recovery by alleviating neuroinflammation and glutamate excitotoxicity partially via FGF1 . | STEM CELL RESEARCH & THERAPY , 2022 , 13 (1) . |
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Abstract ：
A phytochemical study was carried out on the extract of Trillium tschonoskii rhizomes, resulting in the isolation of thirty-six steroidal glycosides (1-36). Their structures were established mainly by spectroscopic analyses as well as necessary chemical evidence, of which 1-25 were identified as new analogues. Herein, all the isolated ana-logues were screened for the cytotoxicity against intrahepatic cholangiocarcinoma (ICC) cell lines of HuCCT1 and RBE through tumor colony formation and CCK-8 survival analysis, and the results demonstrated that three compounds 9, 12, and 26 significantly repressed tumor colony and sphere formation in both cell lines, respec-tively. Furthermore, the three analogues possessed a remarkable inhibitory role of organoid formation estab-lished from hydrodynamic induced mouse primary intrahepatic cholangiocarcinoma. Moreover, the functional assays of flow cytometry analysis, cancer stemness related gene expression, and western blotting assays all indicated that compound 26 could significantly repress cancer stem markers. Taken together, these results demonstrate that steroidal glycosides derived from T. tschonoskii rhizomes could be potentially implicated in human ICC therapy.
Keyword ：
Intrahepatic cholangiocarcinoma Intrahepatic cholangiocarcinoma Cancer stem cells Cancer stem cells Melanthiaceae Melanthiaceae Steroidal saponin Steroidal saponin Trillium tschonoskii Trillium tschonoskii Organoids Organoids
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| GB/T 7714 | Pang, Xu , Wan, Ling-fei , Yang, Jie et al. Steroidal saponins from Trillium tschonoskii rhizome repress cancer stemness and proliferation of intrahepatic cholangiocarcinoma [J]. | BIOORGANIC CHEMISTRY , 2022 , 121 . |
| MLA | Pang, Xu et al. "Steroidal saponins from Trillium tschonoskii rhizome repress cancer stemness and proliferation of intrahepatic cholangiocarcinoma" . | BIOORGANIC CHEMISTRY 121 (2022) . |
| APA | Pang, Xu , Wan, Ling-fei , Yang, Jie , Bai, Pei-ying , Zhang, Jie , Chen, Xiao-juan et al. Steroidal saponins from Trillium tschonoskii rhizome repress cancer stemness and proliferation of intrahepatic cholangiocarcinoma . | BIOORGANIC CHEMISTRY , 2022 , 121 . |
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Abstract ：
Background Altered lipid metabolism is closely related to the occurrence and development of hepatocellular carcinoma (HCC). Carnitine palmitoyltransferase 1C (CPT1C) is a member of CPT1 family and plays a key role in cancer development and progression. However, how microRNAs (miRNAs) regulate CPT1C-mediated fatty acid transport and oxidation remains to be elucidated. Methods Oil Red O staining, mitochondrial, and lipid droplets immunofluorescence staining were used to detect the functions of miR-377-3p and CPT1C in fatty acid oxidation. Colocalization of palmitate and mitochondria was performed to investigate the function of miR-377-3p and CPT1C in fatty acid transport into mitochondria. Fatty acid oxidation (FAO) assay was used to detect the function of miR-377-3p and CPT1C in FAO. Cell proliferation, migration and invasion assays and animal experiments were used to evaluate the role of miR-377-3p/CPT1C axis in HCC progression in vitro and in vivo. Immunofluorescence staining was used to identify the clinical significance of miR-377-3p and CPT1C in HCC patients. Results MiR-377-3p inhibits CPT1C expression by targeting its 3'-untranslated region. Through repression of CPT1C, miR-377-3p suppresses fatty acid oxidation by preventing fatty acid from entering into mitochondria and decreasing ATP production in HCC cells. Inhibiting fatty acid oxidation abolishes the ability of miR-377-3p/CPT1C axis to regulate HCC proliferation, migration, invasion and metastasis in vitro and in vivo. In HCC patients, CPT1C is significantly upregulated, and miR-377-3p expression and lipid droplets are negatively correlated with CPT1C expression. High expression of miR-377-3p and CPT1C predict better and worse clinical outcomes, respectively. Conclusions We uncover the key function and the relevant mechanisms of the miR-377-3p/CPT1C axis in HCC, which might provide a potential target for the treatment of HCC.
Keyword ：
Fatty acid oxidation Fatty acid oxidation Tumor growth Tumor growth CPT1C CPT1C miR-377-3p miR-377-3p Metastasis Metastasis Hepatocellular carcinoma Hepatocellular carcinoma
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| GB/T 7714 | Zhang, Ting , Zhang, Yanan , Liu, Jie et al. MicroRNA-377-3p inhibits hepatocellular carcinoma growth and metastasis through negative regulation of CPT1C-mediated fatty acid oxidation [J]. | CANCER & METABOLISM , 2022 , 10 (1) . |
| MLA | Zhang, Ting et al. "MicroRNA-377-3p inhibits hepatocellular carcinoma growth and metastasis through negative regulation of CPT1C-mediated fatty acid oxidation" . | CANCER & METABOLISM 10 . 1 (2022) . |
| APA | Zhang, Ting , Zhang, Yanan , Liu, Jie , Ma, Yan , Ye, Qinong , Yan, Xinlong et al. MicroRNA-377-3p inhibits hepatocellular carcinoma growth and metastasis through negative regulation of CPT1C-mediated fatty acid oxidation . | CANCER & METABOLISM , 2022 , 10 (1) . |
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Abstract ：
Aims: Intrahepatic cholangiocarcinoma (ICC) is a highly malignant and heterogeneous cancer with a poor prognosis. At present, there is no optimal treatment except for surgical resection, and recurrence after resection will lead to death due to multidrug resistance. Changes in the redox signal have been found to be closely related to the growth and drug resistance of tumor cells. Therefore, the purpose of this study was to screen small molecule compounds from the redox library to find a drug for anti-ICC and to explore its downstream mechanism. Material and methods: Tumor clone and sphere formation of ICC cell lines, as well as mouse ICC organoid proliferation assays were utilized to screen the candidate drug in the Redox library. Western blotting, quantitative reverse-transcription polymerase chain reaction (qRT-PCR), as well as cell apoptosis and cell cycle flow cytometry assays were used to explore the mechanism. Results: We found that Hinokitiol was a candidate drug through inhibition of tumor clone and sphere formation, and the expression of cancer stem cell (CSC)-related genes. Furthermore, Hinokitiol significantly inhibited the proliferation of ICC cells by downregulating the ERK and P38 pathways. In addition, the combination of Hinokitiol and Palbociclib showed a significant inhibitory effect on human ICC cells and mouse ICC organoids. Conclusion: Hinokitiol may have the potential to be developed as a clinical therapeutic drug for ICC treatment.
Keyword ：
Redox library Redox library Hinokitiol Hinokitiol Intrahepatic cholangiocarcinoma Intrahepatic cholangiocarcinoma Tumor organoids Tumor organoids Proliferation Proliferation Tumor sphere Tumor sphere
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| GB/T 7714 | Bai, Peiying , Ge, Chen , Yang, Hui et al. Screening a redox library identifies the anti-tumor drug Hinokitiol for treating intrahepatic cholangiocarcinoma [J]. | FRONTIERS IN BIOSCIENCE-LANDMARK , 2022 , 27 (1) . |
| MLA | Bai, Peiying et al. "Screening a redox library identifies the anti-tumor drug Hinokitiol for treating intrahepatic cholangiocarcinoma" . | FRONTIERS IN BIOSCIENCE-LANDMARK 27 . 1 (2022) . |
| APA | Bai, Peiying , Ge, Chen , Yang, Hui , Chen, Haixu , Wan, Lingfei , Zhang, Yuchen et al. Screening a redox library identifies the anti-tumor drug Hinokitiol for treating intrahepatic cholangiocarcinoma . | FRONTIERS IN BIOSCIENCE-LANDMARK , 2022 , 27 (1) . |
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Abstract ：
Pancreatic cancer (PC) is assumed to be an intimidating and deadly malignancy due to being the leading cause of cancer-led mortality, predominantly affecting males of older age. The overall (5 years) survival rate of PC is less than 9% and is anticipated to be aggravated in the future due to the lack of molecular acquaintance and diagnostic tools for its early detection. Multiple factors are involved in the course of PC development, including genetics, cigarette smoking, alcohol, family history, and aberrant epigenetic signatures of the epigenome. In this review, we will mainly focus on the genetic mutations and epigenetic signature of PC. Multiple tumor suppressor and oncogene mutations are involved in PC initiation, including K-RAS, p53, CDKN2A, and SMAD4. The mutational frequency of these genes ranges from 50 to 98% in PC. The nature of mutation diagnosis is mostly homozygous deletion, point mutation, and aberrant methylation. In addition to genetic modification, epigenetic alterations particularly aberrant hypermethylation and hypomethylation also predispose patients to PC. Hypermethylation is mostly involved in the downregulation of tumor suppressor genes and leads to PC, while multiple genes also represent a hypomethylation status in PC. Several renewable drugs and detection tools have been developed to cope with this aggressive malady, but all are futile, and surgical resection remains the only choice for prolonged survival if diagnosed before metastasis. However, the available therapeutic development is insufficient to cure PC. Therefore, novel approaches are a prerequisite to elucidating the genetic and epigenetic mechanisms underlying PC progression for healthier lifelong survival.
Keyword ：
CDKN2A CDKN2A Aberrant hypermethylation Aberrant hypermethylation p53 p53 Pancreatic cancer Pancreatic cancer KRAS KRAS Aberrant epigenetic signature Aberrant epigenetic signature SMAD4 SMAD4
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| GB/T 7714 | Khan Aamir Ali , Liu Xinhui , Yan Xinlong et al. An overview of genetic mutations and epigenetic signatures in the course of pancreatic cancer progression. [J]. | Cancer metastasis reviews , 2021 , 40 (1) : 245-272 . |
| MLA | Khan Aamir Ali et al. "An overview of genetic mutations and epigenetic signatures in the course of pancreatic cancer progression." . | Cancer metastasis reviews 40 . 1 (2021) : 245-272 . |
| APA | Khan Aamir Ali , Liu Xinhui , Yan Xinlong , Tahir Muhammad , Ali Sakhawat , Huang Hua . An overview of genetic mutations and epigenetic signatures in the course of pancreatic cancer progression. . | Cancer metastasis reviews , 2021 , 40 (1) , 245-272 . |
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Abstract ：
肿瘤组织是由恶性上皮细胞及其周围的基质细胞微环境形成的复杂混合体。在肿瘤的发生发展过程中,肿瘤细胞与肿瘤微环境相互作用相互影响,其中癌相关成纤维细胞(CAF)是肿瘤微环境的重要组成部分。CAF不仅促进肿瘤细胞的增殖与转移、肿瘤微血管生成以及耐药性产生,还能抑制机体的抗肿瘤免疫,从而促进肿瘤的恶性进展。本文简要综述癌相关成纤维细胞的特性及其在调控肿瘤发生发展中的作用。
Keyword ：
癌相关成纤维细胞 癌相关成纤维细胞 靶向治疗 靶向治疗 肿瘤微环境 肿瘤微环境
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| GB/T 7714 | 万令飞 , 杨慧 , 葛晨 et al. 癌相关成纤维细胞的特性及其调控肿瘤进程的研究进展 [J]. | 生物技术通讯 , 2020 , 31 (01) : 75-82 . |
| MLA | 万令飞 et al. "癌相关成纤维细胞的特性及其调控肿瘤进程的研究进展" . | 生物技术通讯 31 . 01 (2020) : 75-82 . |
| APA | 万令飞 , 杨慧 , 葛晨 , 刘蕴慧 , 岳文 , 裴雪涛 et al. 癌相关成纤维细胞的特性及其调控肿瘤进程的研究进展 . | 生物技术通讯 , 2020 , 31 (01) , 75-82 . |
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Abstract ：
Pancreatic cancer (PC) is recognized as the most aggressive and deadliest malignancy because it has the highest mortality of all cancers in humans. Mutations in multiple tumor suppressors and oncogenes have been documented to be involved in pancreatic cancer progression and metastasis. The upregulation of tetraspanin 1 (TSPAN1), a transmembrane protein, has been reportedly observed in many human cancers. However, the role of TSPAN1 and its underlying molecular mechanisms in PC progression have not been fully elucidated. In this study, we validated the oncogenic role of TSPAN1 in PC, showing that TSPAN1 reinforces cell proliferation, migration, invasion and tumorigenesis. To investigate the upregulation of TSPAN1 in PC, we showed that miR-216a is the upstream negative regulator of TSPAN1 via direct binding to the TSPAN13'-untranslated region. Through RNA-Seq analysis, we for the first time revealed that TSPAN1 expression transcriptionally regulates ITGA2, which is involved in the actin cytoskeleton pathway. The stimulated cell proliferation and invasion initiated by TSPAN 1 overexpression could be abolished by knockdown of ITGA2 in PC cells. Furthermore, TSPAN1 epigenetically regulates the expression of ITGA2 by modulating the levels of TET2 DNMT3B and DNMT1, resulting in hypomethylation of the CpG island of the ITGA2 promoter. In conclusion, the newly identified miR-216a/TSPAN1/ITGA2 axis is involved in the modulation of PC progression and represents a novel therapeutic strategy for future pancreatic cancer treatment.
Keyword ：
ITGA2 ITGA2 DNA methylation DNA methylation TSPAN1 TSPAN1 Pancreatic cancer Pancreatic cancer miR-216a miR-216a
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| GB/T 7714 | Wang, Shensen , Liu, Xinhui , Khan, Aamir Ali et al. miR-216a-mediated upregulation of TSPAN1 contributes to pancreatic cancer progression via transcriptional regulation of ITGA2 [J]. | AMERICAN JOURNAL OF CANCER RESEARCH , 2020 , 10 (4) : 1115-1129 . |
| MLA | Wang, Shensen et al. "miR-216a-mediated upregulation of TSPAN1 contributes to pancreatic cancer progression via transcriptional regulation of ITGA2" . | AMERICAN JOURNAL OF CANCER RESEARCH 10 . 4 (2020) : 1115-1129 . |
| APA | Wang, Shensen , Liu, Xinhui , Khan, Aamir Ali , Li, Huan , Tahir, Muhammad , Yan, Xinlong et al. miR-216a-mediated upregulation of TSPAN1 contributes to pancreatic cancer progression via transcriptional regulation of ITGA2 . | AMERICAN JOURNAL OF CANCER RESEARCH , 2020 , 10 (4) , 1115-1129 . |
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Background & Aims: Intrahepatic cholangiocarcinoma (ICC) is the second most common liver malignancy. ICC typically features remarkable cellular heterogeneity and a dense stromal reaction. Therefore, a comprehensive understanding of cellular diversity and the interplay between malignant cells and niche cells is essential to elucidate the mechanisms driving ICC progression and to develop therapeutic approaches. Methods: Herein, we performed single-cell RNA sequencing (scRNA-seq) analysis on unselected viable cells from 8 human ICCs and adjacent samples to elucidate the comprehensive transcriptomic landscape and intercellular communication network. Additionally, we applied a negative selection strategy to enrich fibroblast populations in 2 other ICC samples to investigate fibroblast diversity. The results of the analyses were validated using multiplex immunofluorescence staining, bulk transcriptomic datasets, and functional in vitro and in vivo experiments. Results: We sequenced a total of 56,871 single cells derived from human ICC and adjacent tissues and identified diverse tumor, immune, and stromal cells. Malignant cells displayed a high degree of inter-tumor heterogeneity. Moreover, tumor-infiltrating CD4 regulatory T cells exhibited highly immunosuppressive characteristics. We identified 6 distinct fibroblast subsets, of which the majority were CD146-positive vascular cancer-associated fibroblasts (vCAFs), with highly expressed microvasculature signatures and high levels of interleukin (IL)-6. Functional assays indicated that IL-6 secreted by vCAFs induced significant epigenetic alterations in ICC cells, particularly upregulating enhancer of zeste homolog 2 (EZH2) and thereby enhancing malignancy. Furthermore, ICC cell-derived exosomal miR-9-5p elicited high expression of IL-6 in vCAFs to promote tumor progression. Conclusions: Our single-cell transcriptomic dataset delineates the inter-tumor heterogeneity of human ICCs, underlining the importance of intercellular crosstalk between ICC cells and vCAFs, and revealing potential therapeutic targets. Lay summary: Intrahepatic cholangiocarcinoma is an aggressive and chemoresistant malignancy. Better understanding the complex transcriptional architecture and intercellular crosstalk of these tumors will help in the development of more effective therapies. Herein, we have identified important interactions between cancer cells and cancer-associated fibroblasts in the tumor stroma, which could have therapeutic implications. (C) 2020 European Association for the Study of the Liver. Published by Elsevier B.V.
Keyword ：
Single-cell RNA sequencing Single-cell RNA sequencing Tumor heterogeneity Tumor heterogeneity CD146 CD146 Intrahepatic cholangiocarcinoma Intrahepatic cholangiocarcinoma Cancer-associated fibroblasts Cancer-associated fibroblasts
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| GB/T 7714 | Zhang, Min , Yang, Hui , Wan, Lingfei et al. Single-cell transcriptomic architecture and intercellular crosstalk of human intrahepatic cholangiocarcinoma [J]. | JOURNAL OF HEPATOLOGY , 2020 , 73 (5) : 1118-1130 . |
| MLA | Zhang, Min et al. "Single-cell transcriptomic architecture and intercellular crosstalk of human intrahepatic cholangiocarcinoma" . | JOURNAL OF HEPATOLOGY 73 . 5 (2020) : 1118-1130 . |
| APA | Zhang, Min , Yang, Hui , Wan, Lingfei , Wang, Zhaohai , Wang, Haiyang , Ge, Chen et al. Single-cell transcriptomic architecture and intercellular crosstalk of human intrahepatic cholangiocarcinoma . | JOURNAL OF HEPATOLOGY , 2020 , 73 (5) , 1118-1130 . |
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Abstract ：
BackgroundGlioblastoma (GBM) is the most common type of primary malignant brain tumor. Molecular hydrogen has been considered a preventive and therapeutic medical gas in many diseases including cancer. In our study, we sought to assess the potential role of molecular hydrogen on GBM.MethodsThe in vivo studies were performed using a rat orthotopic glioma model and a mouse subcutaneous xenograft model. Animals inhaled hydrogen gas (67%) 1h two times per day. MR imaging studies were performed to determine the tumor volume. Immunohistochemistry (IHC), immunofluorescence staining, and flow cytometry analysis were conducted to determine the expression of surface markers. Sphere formation assay was performed to assess the cancer stem cell self-renewal capacity. Assays for cell migration, invasion, and colony formation were conducted.ResultsThe in vivo study showed that hydrogen inhalation could effectively suppress GBM tumor growth and prolong the survival of mice with GBM. IHC and immunofluorescence staining demonstrated that hydrogen treatment markedly downregulated the expression of markers involved in stemness (CD133, Nestin), proliferation (ki67), and angiogenesis (CD34) and also upregulated GFAP expression, a marker of differentiation. Similar results were obtained in the in vitro studies. The sphere-forming ability of glioma cells was also suppressed by hydrogen treatment. Moreover, hydrogen treatment also suppressed the migration, invasion, and colony-forming ability of glioma cells.ConclusionsTogether, these results indicated that molecular hydrogen may serve as a potential anti-tumor agent in the treatment of GBM.
Keyword ：
Glioma stem-like cell Glioma stem-like cell Cancer cell stemness Cancer cell stemness Molecular hydrogen Molecular hydrogen Glioblastoma Glioblastoma
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| GB/T 7714 | Liu, Meng-yu , Xie, Fei , Zhang, Yan et al. Molecular hydrogen suppresses glioblastoma growth via inducing the glioma stem-like cell differentiation [J]. | STEM CELL RESEARCH & THERAPY , 2019 , 10 . |
| MLA | Liu, Meng-yu et al. "Molecular hydrogen suppresses glioblastoma growth via inducing the glioma stem-like cell differentiation" . | STEM CELL RESEARCH & THERAPY 10 (2019) . |
| APA | Liu, Meng-yu , Xie, Fei , Zhang, Yan , Wang, Ting-ting , Ma, Sheng-nan , Zhao, Peng-xiang et al. Molecular hydrogen suppresses glioblastoma growth via inducing the glioma stem-like cell differentiation . | STEM CELL RESEARCH & THERAPY , 2019 , 10 . |
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