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摘要 ：
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.
关键词 ：
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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摘要 ：
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.
关键词 ：
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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摘要 ：
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.
关键词 ：
Aberrant hypermethylation Aberrant hypermethylation Aberrant epigenetic signature Aberrant epigenetic signature CDKN2A CDKN2A p53 p53 KRAS KRAS Pancreatic cancer Pancreatic cancer 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 AND 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 AND 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 AND METASTASIS REVIEWS , 2021 , 40 (1) , 245-272 . |
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摘要 ：
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.
关键词 ：
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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摘要 ：
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.
关键词 ：
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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摘要 ：
我国“双一流”建设目标的实现以高素质的高校教师队伍为基础,更需合理的激励制度进行维护与保障.教师职称晋升作为高校教师评聘环节中最为重要的激励制度,对教师发展有明确的导向作用.本研究梳理了教师发展的内涵、理念与作用,建立了教师发展视域下的政策分析框架与标准,并采用案例法对北京市两所一流学科建设院校的教师职称评审政策文本从完整度、清晰度和适切性上进行了理念与使命、结构与内容、方法与程序、反馈与改进四个方面的分析,并提出了相应的问题与政策建议.
关键词 ：
双一流 双一流 政策分析 政策分析 教师发展 教师发展 职称评审 职称评审
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| GB/T 7714 | 阎新龙 , 莫蕾钰 , 张琳 . 教师发展视域下北京一流学科建设高校教师职称评审政策分析——基于两所高校的案例 [J]. | 中国地质教育 , 2019 , 28 (3) : 9-14 . |
| MLA | 阎新龙 et al. "教师发展视域下北京一流学科建设高校教师职称评审政策分析——基于两所高校的案例" . | 中国地质教育 28 . 3 (2019) : 9-14 . |
| APA | 阎新龙 , 莫蕾钰 , 张琳 . 教师发展视域下北京一流学科建设高校教师职称评审政策分析——基于两所高校的案例 . | 中国地质教育 , 2019 , 28 (3) , 9-14 . |
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摘要 ：
Cancer stem-like cells (CSCs) are critical for the initiation, progression, chemoresistance and postsurgical recurrence of liver cancer. They are thought to be novel targets for the treatment of liver cancer, however, efficient agents that target liver cancer stem cells (CSCs) have not been identified. MicroRNAs (miRNAs) are small non-coding RNAs that target the 3untranslated region (3UTR) of mRNAs. Their dysregulation has been implicated in several types of cancer including liver cancer, but it still remains unknown if they play a role in targeting liver CSCs. We compared the miRNA profiles between liver cancer samples and adjacent non-tumor tissues using The Cancer Genome Atlas (TCGA) datasets. Several miRNAs including miR-486-5p (miR-486) were found to be significantly downregulated in liver cancer tissues. These differentially expressed miRNAs were screened between CSC-enriched tumor spheres and adherent cells. miR-486 was significantly downregulated in tumor spheres and liver cancer samples. Ectopic expression of miR-486 significantly repressed the self-renewal and invasion of CSCs in vitro and tumorigenesis in vivo. Notably, we found that sirtuin 1 (Sirt1) served as a direct target of miR-486. The high expression of Sirt1 was involved in maintaining the self-renewal and tumorigenic potential of liver CSCs. The results of the present study indicated that the miR-486-Sirt1 axis was involved in suppressing CSC traits and tumor progression.
关键词 ：
liver cancer liver cancer cancer stem cells cancer stem cells miR-486 miR-486 Sirt1 Sirt1
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| GB/T 7714 | Yan, Xinlong , Liu, Xinhui , Wang, Zhaohai et al. MicroRNA-486-5p functions as a tumor suppressor of proliferation and cancer stem-like cell properties by targeting Sirt1 in liver cancer [J]. | ONCOLOGY REPORTS , 2019 , 41 (3) : 1938-1948 . |
| MLA | Yan, Xinlong et al. "MicroRNA-486-5p functions as a tumor suppressor of proliferation and cancer stem-like cell properties by targeting Sirt1 in liver cancer" . | ONCOLOGY REPORTS 41 . 3 (2019) : 1938-1948 . |
| APA | Yan, Xinlong , Liu, Xinhui , Wang, Zhaohai , Cheng, Qian , Ji, Guanghong , Yang, Hui et al. MicroRNA-486-5p functions as a tumor suppressor of proliferation and cancer stem-like cell properties by targeting Sirt1 in liver cancer . | ONCOLOGY REPORTS , 2019 , 41 (3) , 1938-1948 . |
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摘要 ：
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.
关键词 ：
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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摘要 ：
Accumulating evidence suggests that Ras GTPase-activating protein SH3 domain-binding protein 1 (G3BP1) is very crucial to regulate tumorigenesis and metastasis. Recently, many research works have suggested that G3BP1 is overexpressed in many human cancers including esophageal cancer. Nevertheless, the functional roles of G3BP1 in esophageal cancer are still unknown. Here, the results suggested that silencing of G3BP1 inhibited proliferation, migration, and invasion of esophageal cancer cells, whereas overexpression of G3BP1 led to opposite effects on the growth and metastasis. Surprisingly, G3BP1-depletion had no effect on cell death but caused the arrest of cell cycle in the G(0)/G(1) phase and increased the levels of p53 and p21. In addition, loss of G3BP1 led to a significant elevation of E-cadherin and decrease of N-cadherin, Vimentin, Snail, MMP-9, and MMP-2. Mechanistically, loss of G3BP1 dramatically suppressed Wnt-stimulated T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factor activity and downregulated its target genes including c-Myc, Axin2, and cyclin D1. Moreover, knockdown of G3BP1 downregulated the expression levels of p-PI3K, p-AKT, and p-GSK-3 beta, but the total PI3K, AKT, and GSK-3 beta were not changed. Furthermore, our data proved that the promoting effects of G3BP1-overexpression on cell proliferation, migration, and invasion could be rescued by PI3K inhibitor LY294002 treatment. Collectively, our results here elucidate that G3BP1-depletion suppresses proliferation, migration, and invasion capabilities of esophageal cancer cells via the inactivation of Wnt/beta-catenin and PI3K/AKT signaling pathways. Furthermore, our findings imply that G3BP1 can participate in the regulation of esophageal cancer progression, and will be taken as a promising target to treat esophageal cancer.
关键词 ：
esophageal cancer esophageal cancer Wnt/beta-catenin Wnt/beta-catenin PI3K/AKT PI3K/AKT G3BP1 G3BP1 epithelial-mesenchymal transition (EMT) epithelial-mesenchymal transition (EMT)
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| GB/T 7714 | Zhang, Li-Na , Zhao, Lei , Yan, Xin-Long et al. Loss of G3BP1 suppresses proliferation, migration, and invasion of esophageal cancer cells via Wnt/beta-catenin and PI3K/AKT signaling pathways [J]. | JOURNAL OF CELLULAR PHYSIOLOGY , 2019 , 234 (11) : 20469-20484 . |
| MLA | Zhang, Li-Na et al. "Loss of G3BP1 suppresses proliferation, migration, and invasion of esophageal cancer cells via Wnt/beta-catenin and PI3K/AKT signaling pathways" . | JOURNAL OF CELLULAR PHYSIOLOGY 234 . 11 (2019) : 20469-20484 . |
| APA | Zhang, Li-Na , Zhao, Lei , Yan, Xin-Long , Huang, Ying-Hui . Loss of G3BP1 suppresses proliferation, migration, and invasion of esophageal cancer cells via Wnt/beta-catenin and PI3K/AKT signaling pathways . | JOURNAL OF CELLULAR PHYSIOLOGY , 2019 , 234 (11) , 20469-20484 . |
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摘要 ：
本发明提出了新的靶向肿瘤微环境与肺癌干细胞相互作用的miRNA的检测及应用，并提出了试剂在制备药物中的用途。该药物用于下列的至少之一：预防或治疗癌症，抑制癌症干细胞球的形成或增殖，抑制体内癌症的形成或增殖，该药物用于预防或治疗癌症，所述试剂用于过表达核酸，所述核酸具有下列的核苷酸序列：1)SEQ ID NO：1所示的核苷酸序列；2)具有与SEQ ID NO：1所示的核苷酸序列至少70％、至少75％、至少80％、至少85％、至少90％、至少95％、至少99％同一性；或3)3)与1)相比具有一个或者多个核苷酸的突变。
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| GB/T 7714 | 阎新龙 , 岳文 , 裴雪涛 et al. 新的靶向肿瘤微环境与肺癌干细胞相互作用的miRNA的检测及应用 : CN201810388252.4[P]. | 2018-04-26 . |
| MLA | 阎新龙 et al. "新的靶向肿瘤微环境与肺癌干细胞相互作用的miRNA的检测及应用" : CN201810388252.4. | 2018-04-26 . |
| APA | 阎新龙 , 岳文 , 裴雪涛 , 刘馨慧 , 杨慧 , 万令飞 et al. 新的靶向肿瘤微环境与肺癌干细胞相互作用的miRNA的检测及应用 : CN201810388252.4. | 2018-04-26 . |
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