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1.
肿瘤微环境主要由肿瘤细胞、肿瘤相关间质细胞及细胞外基质组成。肿瘤细胞通过多种方式调控肿瘤微环境中的间质细胞,诱导间质细胞分化并发挥促肿瘤的作用,从而为肿瘤的生长及转移创造一个适宜的环境。DNA甲基化异常是肿瘤的特点。目前关于肿瘤的甲基化调控机制已有大量报道,对于肿瘤细胞与微环境中间质细胞的相互作用机制也有了一些报道。然而,关于肿瘤细胞对微环境间质细胞的甲基化调控机制以及这种调控对肿瘤发生发展的影响并没有系统的论述。本综述总结了肿瘤细胞对微环境中间质细胞甲基化调控机制的最新研究进展,以及间质细胞发生的一些促肿瘤改变,从而全面阐释了肿瘤细胞和间质细胞间的相互作用,同时总结了肿瘤细胞对肿瘤微环境的表观遗传学调控,尤其是甲基化调控在肿瘤进展中发挥了重要的作用。干预肿瘤细胞对微环境中间质细胞的甲基化调节过程,可以发挥抗肿瘤的作用。  相似文献   

2.
肿瘤转移的分子基础   总被引:1,自引:0,他引:1  
转移是癌瘤细胞离开原发灶后在体内其它部位停留增殖的复杂过程.侵袭、播散、存活、增殖的转移过程中涉及一系列瘤细胞与机体微环境的相互作用,许多因子参与了转移的维持和发展.本文着重介绍参与转移的几个重要分子,如纤溶酶原激活物和抑制物、基质金属蛋白酶、以及调节转移的几个转移抑制基因的作用机制.肿瘤转移的分子生物学进展,有可能导致新的靶向治疗的开展.  相似文献   

3.
新型抗凋亡基因Survivin与肿瘤的研究进展   总被引:2,自引:0,他引:2  
综述Survivin是一种新型凋亡抑制因子,主要通过抑制Caspase-3和Caspase-7的活性而阻断细胞凋亡过程。指出Survivin选择性地表达于胚胎发育组织和大多数肿瘤组织,而正常成人分化组织中不表达。认为Survivin参与了细胞周期调控,与肿瘤的发展和血管形成有关,可作为肿瘤治疗的新靶点。  相似文献   

4.
非编码小分子RNA(miRNA)是一类内生的、参与基因转录后水平调控的RNA。研究表明,miRNA具有调控细胞增殖、分化、凋亡、个体发育等生物学功能,并与肿瘤的发生密切相关。本文概述了miRNA的产生、生物学特性、在肿瘤发生过程中的作用以及在癌症诊疗中的应用价值。  相似文献   

5.
MicroRNA在乳腺癌发展过程中的作用机制及临床应用分析   总被引:2,自引:0,他引:2  
概搜集已报道的在乳腺癌发生发展过程中有重要作用的microRNA信息,结合相关肿瘤模型的实验数据,评估microRNA在乳腺癌诊断和治疗方面的应用前景。以“癌基因”和“癌抑制基因”为分类依据,全面地总结归纳乳腺癌相关microRNA的功能和作用机制,进一步从临床诊断标记物和治疗靶点的层面分析microRNA的潜在临床应用价值。表1和2总结了microRNA参与乳腺癌发展过程的具体事件及其调控的靶基因。同时,本文还深入探讨microRNA作为临床诊断标记物及治疗靶点的可行性,揭示已有研究的不足之处,为今后的相关工作方向提供一些建议。  相似文献   

6.
肿瘤转移小鼠模型研究进展   总被引:1,自引:0,他引:1  
目前已有若干小鼠模型系统应用于分析肿瘤转移过程。这些模型可以为肿瘤进展、血管形成、局部浸润等转移时相提供可靠的解释,有助于揭示肿瘤转移机制。其中应用最为广泛的肿瘤转移小鼠模型包括遗传工程小鼠模型和可移植肿瘤小鼠模型。在肿瘤转移研究中,基于遗传学和分子生物学的综合研究方法是研究转移性癌症细胞或转移瘤微环境的有效手段。  相似文献   

7.
目的:研究肝癌细胞缺氧微环境导致mi R-210表达变化与肿瘤进展、预后等相关性。创新点:首次阐明了mi R-210表达与肝癌预后及缺氧相关基因的关系。方法:选取肿瘤基因数据库(TCGA)中424位肝癌患者的mi R-210表达水平、临床病理参数及缺氧相关基因(HIF1α、HIF3α、PTPN1和BNIP3)表达量,研究mi R-210与肝癌预后及缺氧基因之间的相关性。结论:mi R-210的表达与肝细胞癌进展分期呈正相关,它的高表达预示更低的无瘤生存率。因此,推测mi R-210可能与肿瘤细胞缺氧相关性死亡有关。  相似文献   

8.
《生物学教学》2014,(6):76-77
据2013年12月23日《科技日报》报道,中国科学技术大学吴缅和梅一德教授研究组揭示了长片段非编码RNA通过调控肿瘤细胞瓦伯格效应促进肿瘤生长的机制。相关研究在线发表在《分子细胞》杂志上。  相似文献   

9.
抑癌基因是人类正常细胞中所具有的一类基因,对细胞的增殖分化有调节作用。染色体体臂上某一区域非随机杂合性缺失导致抑癌基因的丧失,从而促使肿瘤发生。本文总结了第17号染色体短臂(17p)杂合性缺失与肿瘤发生关系的研究进展,该研究不仅为我们定位新的抑癌基因提供了基础,为肿瘤的预防、早期发现和诊断提供了依据,同时也使我们能更好理解肿瘤的分子进展。  相似文献   

10.
肿瘤干细胞是肿瘤中一些数量极少,具有自我更新能力和不定分化潜能、驱使肿瘤形成的细胞.这些细胞具有干细胞特性,近年来,发现肿瘤干细胞与消化系统肿瘤的起源、发生和演进有关.为此,就肿瘤干细胞与消化系统肿瘤的相关研究进展做一综述.  相似文献   

11.

Osteosarcoma (OS) is the most common primary bone tumor in children and adolescents. It is an aggressive tumor with a tendency to spread to the lung, which is the most common site of metastasis. Patients with advanced OS with metastases have poor prognoses despite the application of chemotherapy, thus highlighting the need for novel therapeutic targets. The tumor microenvironment (TME) of OS is confirmed to be essential for and supportive of tumor growth and dissemination. The immune component of the OS microenvironment is mainly composed of tumor-associated macrophages (TAMs). In OS, TAMs promote tumor growth and angiogenesis and upregulate the cancer stem cell-like phenotype. However, TAMs inhibit the metastasis of OS. Therefore, much attention has been paid to investigating the mechanism of TAMs in OS development and the progression of immunotherapy for OS. In this article, we aim to summarize the roles of TAMs in OS and the major findings on the application of TAMs in OS treatment.

  相似文献   

12.
The tumor microenvironment (TME) plays an important role in supporting cancer progression. The TME is composed of tumor cells, the surrounding tumor-associated stromal cells, and the extracellular matrix (ECM). Crosstalk between the TME components contributes to tumorigenesis. Recently, one of our studies showed that pancreatic ductal adenocarcinoma (PDAC) cells can induce DNA methylation in cancer-associated fibroblasts (CAFs), thereby modifying tumor-stromal interactions in the TME, and subsequently creating a TME that supports tumor growth. Here we summarize recent studies about how DNA methylation affects tumorigenesis through regulating tumorassociated stromal components including fibroblasts and immune cells. We also discuss the potential for targeting DNA methylation for the treatment of cancers.  相似文献   

13.
MicroRNAs (miRNAs or miRs) are endogenous non-coding RNAs that negatively regulate gene expression by binding to the 3′ non-coding regions of target mRNAs, resulting in their cleavage or blocking their translation. miRNAs may have an impact on cell differentiation, proliferation, and survival, and their deregulation can be inclined to diseases and cancers, including thyroid tumors. The purpose of this review is to summarize the existing findings of deregulated miRNAs in different types of thyroid tumors and to exhibit their potential target genes, especially to demonstrate those involved in tumor invasion and metastasis. In addition, new findings of circulating miRNA expression profiles, single nucleotide polymorphism (SNP) in thyroid tumors, and the correlation of somatic mutations with deregulated miRNA expression in thyroid tumors were all included in this review.  相似文献   

14.
Zhu  Wei  Zhou  Bo-lun  Rong  Li-juan  Ye  Li  Xu  Hong-juan  Zhou  Yao  Yan  Xue-jun  Liu  Wei-dong  Zhu  Bin  Wang  Lei  Jiang  Xing-jun  Ren  Cai-ping 《Journal of Zhejiang University. Science. B》2020,21(2):122-136

Polypyrimidine tract-binding protein 1 (PTBP1) plays an essential role in splicing and is expressed in almost all cell types in humans, unlike the other proteins of the PTBP family. PTBP1 mediates several cellular processes in certain types of cells, including the growth and differentiation of neuronal cells and activation of immune cells. Its function is regulated by various molecules, including microRNAs (miRNAs), long non-coding RNAs (IncRNAs), and RNA-binding proteins. PTBP1 plays roles in various diseases, particularly in some cancers, including colorectal cancer, renal cell cancer, breast cancer, and glioma. In cancers, it acts mainly as a regulator of glycolysis, apoptosis, proliferation, tumorigenesis, invasion, and migration. The role of PTBP1 in cancer has become a popular research topic in recent years, and this research has contributed greatly to the formulation of a useful therapeutic strategy for cancer. In this review, we summarize recent findings related to PTBP1 and discuss how it regulates the development of cancer cells.

  相似文献   

15.
16.
Mesenchymal stem cells (MSCs) are plastic-adherent cells with a characteristic surface phenotype and properties of self-renewal, differentiation, and high proliferative potential. The characteristics of MSCs and their tumortropic capability make them an ideal tool for use in cell-based therapies for cancer, including glioma. These cells can function either through a bystander effect or as a delivery system for genes and drugs. MSCs have been demonstrated to inhibit the growth of glioma and to improve survival following transplantation into the brain. We briefly review the current data regarding the use of MSCs in the treatment of glioma and discuss the potential strategies for development of a more specific and effective therapy.  相似文献   

17.
In vitro study of immunosuppressive effect of apoptotic cells   总被引:3,自引:0,他引:3  
INTRODUCTION Apoptosis plays an important role in differen- tiation, development and pathophysiological proc- esses such as inflammation, neoplasia and autoim- mune diseases. For a long time, apoptotic cells per se and the clearance of apoptotic cells had been viewed as neutral in immune response. Recently many in- vestigations suggested that apoptotic cells actively regulate the immune response (Voll et al., 1997; Fadok et al., 1998; 2000; Byrne and Reen, 2002). Apoptotic cells release …  相似文献   

18.
Objective: To investigate molecular alterations associating with prostate carcinoma progression and potentially provide information toward more accurate prognosis/diagnosis. Methods: A set of laser captured microdissected (LCM) specimens from 300 prostate cancer (PCa) patients undergoing radical prostatectomy (RP) were defined. Ten patients representing "aggressive" PCa, and 10 representing "non-aggressive" PCa were selected based on prostate-specific antigen (PSA) recurrence,Gleason score, pathological stage and tumor cell differentiation, with matched patient age and race between the two groups.Normal and neoplastic prostate epithelial cells were collected with LCM from frozen tissue slides obtained from the RP specimens.The expressions of a panel of genes, including NPY, PTEN, AR,AMACR, DD3, and GSTP1, were measured by quantitative real-time RT-PCR (TaqMan), and correlation was analyzed with clinicopathological features. Results: The expressions of AMACR and DD3 were consistently up-regulated in cancer cells compared to benign prostate epithelial cells in all PCa patients, whereas GSTP1 expression was down regulated in each patient. NPY, PTEN and AR exhibited a striking difference in their expression patterns between aggressive and non-aggressive PCas (P=0.0203, 0.0284, and 0.0378, respectively, Wilcoxon rank sum test). The lower expression of NPY showed association with "aggressive" PCas based on a larger PCa patient cohort analysis (P=0.0037,univariate generalized linear model (GLM) analysis). Conclusion: Despite widely noted heterogeneous nature of PCa, gene expression alterations of AMACR, DD3, and GSTP1 in LCM-derived PCa epithelial cells suggest for common underlying mechanisms in the initiation of PCa. Lower NPY expression level is significantly associated with more aggressive clinical behavior of PCa; PTEN and AR may have potential in defining PCa with aggressive clinical behavior. Studies along these lines have potential to define PCa-associated gene expression alterations and likely co-regulation of genes/pathways critical in the biology of PCa onset/progression.  相似文献   

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Recent studies revealed that apoptotic cells are actively involved in immunosuppression and anti-inflammation. After being phagocytosed by macrophages, apoptotic cells can actively regulate cytokines secretion from lipopolysaccharide (LPS)-stimulated macrophages in which the secretion of immunosuppressive cytokines such as interleukin-10 (IL-10) is increased while the pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNFα), interleukin-1beta (IL-1β) and leukin-8 (IL-8) are suppressed. In this paper, we first present evidence that phagocytosed apoptotic cells regulate cytokine secretion of LPS-stimulated macrophages, but also inhibit the activation of T lymphocytes stimulated by ConA. These data suggest that apoptotic cells can alter the biological behavior of macrophages which gain immunosuppressive property. Project supported by the National Basic Research Program (973) of China (No. 2003CB515500) and the National Natural Science Foundation of China (No. 30371358)  相似文献   

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