共查询到20条相似文献,搜索用时 15 毫秒
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Bertolini F 《Cancer metastasis reviews》2008,27(1):95-101
Anti-angiogenic drugs, alone or in combination with chemotherapeutics, are increasingly used by medical oncologists. In many
cases, however, their mechanism of action and the tailoring of optimal dosage/schedule are still elusive. Circulating endothelial
cell (CEC) and progenitor (CEP) number and viability are modulated in a large series of diseases including cancer, and look
promising as surrogate biomarkers for the definition of the optimal biological dose of anti-angiogenic drugs and for patients’
stratification. Along with CECs and CEPs, potential EC- and CEP-related surrogate molecular markers such as VE-Cadherin and
CD133 are currently under preclinical and clinical investigation. 相似文献
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Bonnie F. Sloane Kamiar Moin Evzen Krepela Jurij Rozhin 《Cancer metastasis reviews》1990,9(4):333-352
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Armando Rojas Cristian Lindner Iv n Schneider Ileana Gonz lez Hernan Araya Erik Morales Milibeth G mez Nelson Urdaneta Paulina Araya Miguel Angel Morales 《World journal of gastrointestinal oncology》2021,13(12):1997-2012
Compelling pieces of evidence derived from both clinical and experimental research has demonstrated the crucial contribution of diabetes mellitus (DM) as a risk factor associated with increased cancer incidence and mortality in many human neoplasms, including gastric cancer (GC). DM is considered a systemic inflammatory disease and therefore, this inflammatory status may have profound effects on the tumor microenvironment (TME), particularly by driving many molecular mechanisms to generate a more aggressive TME. DM is an active driver in the modification of the behavior of many cell components of the TME as well as altering the mechanical properties of the extracellular matrix (ECM), leading to an increased ECM stiffening. Additionally, DM can alter many cellular signaling mechanisms and thus favoring tumor growth, invasion, and metastatic potential, as well as key elements in regulating cellular functions and cross-talks, such as the microRNAs network, the production, and cargo of exosomes, the metabolism of cell stroma and resistance to hypoxia. In the present review, we intend to highlight the mechanistic contributions of DM to the remodeling of TME in GC. 相似文献
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粘液性大肠癌组织蛋白酶B、D表达与肿瘤浸润 总被引:1,自引:0,他引:1
目的组织蛋白酶B(Cathepsin B,CB)在粘液性大肠癌的表达尚未明了.组织蛋白酶D(Cathepsin D,CD)在肿瘤浸润和转移中的作用仍存在争议.本实验目的系探讨粘液性大肠癌CB和CD表达及其与肿瘤浸润转移的关系.方法采用免疫组化方法对48例人不同类型大肠癌CB及CD表达进行半定量检测.结果伴淋巴结转移大肠癌CB和CD表达率高于不伴淋巴结转移大肠癌,差异具显著性(P<0.05;P<0.005).粘液性大肠癌CB表达高于非粘液性者,差别具显著性(P<0.05),但CD表达差异却无显著性意义(P>0.05).结论提示大肠癌CB和CD表达与肿瘤浸润转移有关,CB在粘液性大肠癌浸润转移中作用可能更为重要. 相似文献
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We have examined the ability of various components of breast, colorectal and ovarian tumours to regulate the activation and function of LAK cells and TILs, immune effectors which have been used as anti-tumour therapies. Tumour cell or supernatants derived from their short-term in vitro culture, inhibited the activation of PBMC by IL-2 but supported the continued proliferation of LAK or TIL cells which had already been activated. Despite being able to enhance or suppress growth of a range of cell lines, a cell-free, soluble preparation (TDS) from primary tumours was uniformly inhibitory to IL-2 activated cells, suggesting that it reflected the immunoregulatory nature of human tumours more accurately than cell-cultures or their supernatants. 相似文献
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Melanoma arises through the accrual of mutations in genes critical for proliferation and survival. Although melanoma had been
traditionally conceptualized as a cell-autonomous event, increasing evidence supports the notion that these tumors are not
isolated entities but rather depend, interact with, and react to the adjacent microenvironment. Melanoma is composed of not
only the malignant cells but also the supporting stroma, which includes fibroblasts, endothelial cells, immune cells, soluble
molecules, and the extracellular matrix (ECM). Tumor cells actively interact with the microenvironment in a bidirectional
manner through molecular signals that modulate the malignant phenotype. This article briefly reviews the molecular basis of
melanomagenesis as well as the interplay of melanoma with other cells of the tumor microenvironment and components of the
ECM. It also discusses the influence of the microenvironment on therapeutic targeting of melanoma, highlighting recent studies
that propose novel strategies to target tumor-microenvironment interactions. 相似文献
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Objective
We evaluated miR-451 expression in serum and tissue samples of esophageal squamous cell carcinoma (ESCC) patients. Then, we examined a secretory role of miR-451 in esophageal tumor microenvironment.Methods
miR-451 expression was evaluated in 39 serum samples from esophageal SCC patients compared to 39 normal individuals as well as 26 pairs of fresh-frozen tumor and adjacent normal tissues from patients with ESCC, using qRT-PCR. In a co-culture system of human normal fibroblasts (HFSF-PI3) and esophageal cancer cell line (KYSE-30), we evaluated exosomal miR-451 secretion into the conditioned medium (CM) of both cell lines. Then, we analyzed the effect of primiR-451-transfected fibroblasts on the migration potency of their neighboring KYSE-30 cells.Results
We detected miR-451 over-expression in serum samples of esophageal cancer patients compared to the normal group (P = 0.005). Interestingly, fresh-frozen tumor tissues from the same patients showed miR-451 down-regulation compared to their adjacent normal counterparts (P = 0.043). Co-culturing the KYSE-30 cell line with normal fibroblasts significantly induced miR-451 exosomal secretion into the CM. Moreover, co-culture of KYSE-30 cell line with miR-451-over-expressing fibroblasts significantly induced migration tendency in KYSE-30 cell line compared to the mock-transfected fibroblasts (P < 0.0001). In this system, MIF expression (a validated target of miR-451) in the KYSE-30 cell line was increased although this alteration was not statistically significant (fold change = 4.44).Conclusions
Our data suggest that cancer-associated fibroblasts use exosomal miR-451 as a signaling molecule to provide a favorable niche for tumor cell migration and cancer progression. Our findings provide new insights into the stromal role of miR-451 in the esophageal tumor microenvironment as a communicatory molecule and suggest a signaling role for miR-451 in extracellular matrix cross-talks.11.
Encoded by the hepatitis B virus, hepatitis B virus X protein (HBx) is a multifunctional, potentially oncogenic protein that acts primarily during the progression from chronic hepatitis B to cirrhosis and hepatocellular carcinoma (HCC). In recent decades, it has been established that chronic inflammation generates a tumor-supporting microenvironment. HCC is a typical chronic inflammation-related cancer, and inflammation is the main risk factor for HCC progression. The viral transactivator HBx plays a pivotal role in the initiation and maintenance of hepatic inflammatory processes through interactions with components of the tumor microenvironment including tumor cells and the surrounding peritumoral stroma. The complex interactions between HBx and this microenvironment are thought to regulate tumor growth, progression, invasion, metastasis, and angiogenesis. In this review, we have summarized the current evidence evaluating the function of HBx and its contribution to the inflammatory liver tumor microenvironment. 相似文献
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Lee HO Silva AS Concilio S Li YS Slifker M Gatenby RA Cheng JD 《Cancer research》2011,71(20):6327-6337
Interactions between cancer cells and their microenvironment are crucial for promoting tumor growth and invasiveness. In the tumor adaptive landscape model, hypoxic and acidic microenvironmental conditions reduce the fitness of cancer cells and significantly restrict their proliferation. This selects for enhanced motility as cancer cells may evolve an invasive phenotype if the consequent cell movement is rewarded by proliferation. Here, we used an integrative approach combining a mathematical tumor adaptive landscape model with experimental studies to examine the evolutionary dynamics that promote an invasive cancer phenotype. Computer simulation results hypothesized an explicit coupling of motility and proliferation in cancer cells. The mathematical modeling results were also experimentally examined by selecting Panc-1 cells with enhanced motility on a fibroblast-derived 3-dimensional matrix for cells that move away from the unfavorable metabolic constraints. After multiple rounds of selection, the cells that adapted through increased motility were characterized for their phenotypic properties compared with stationary cells. Microarray and gene depletion studies showed the role of Rho-GDI2 in regulating both cell movement and proliferation. Together, this work illustrates the partnership between evolutionary mathematical modeling and experimental validation as a potentially useful approach to study the complex dynamics of the tumor microenvironment. 相似文献
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Morten Busk Stefan WalentaWolfgang Mueller-Klieser Torben SteinicheSteen Jakobsen Michael Robert HorsmanJens Overgaard 《Radiotherapy and oncology》2011,99(3):404-411
Background and purpose
Tumor cells are recognized as being highly glycolytic. However, recently it was suggested that lactate produced in hypoxic tumor areas may be taken up by the monocarboxylate transporter MCT1 and oxidized in well-oxygenated tumor parts. Furthermore, it was shown that inhibition of lactate oxidation using the MCT1 inhibitor α-cyano-hydroxycinnamate (CHC) can radio-sensitize tumors possibly by forcing a switch from lactate oxidization to glycolysis in oxygenated cells, which in turn improves tumor oxygenation and indirectly kills radio-resistant hypoxic tumor cells from glucose starvation.Material and methods
To provide direct evidence for the existence of a targetable energetic symbiosis, mice bearing SiHa or FaDudd tumors were treated with CHC for different time periods. One hour prior to sacrifice, mice were administered with the glucose analog fluorodeoxyglucose (FDG) and the hypoxia-marker pimonidazole. Tumor cryosections were analyzed for regional glucose retention (FDG autoradiograms), hypoxia (pimonidazole retention) and glucose and lactate levels (bioluminescence imaging).Results
Treatment did not influence metabolite concentrations, necrosis or extent of hypoxia, but pixel-by-pixel analysis comparing FDG retention and hypoxia (a measure of the apparent in vivo Pasteur effect) showed that CHC treatment caused a transient reduction in the Pasteur effect in FaDudd 1.5 h following CHC administration whereas a reduction was only observed in SiHa following repeated treatments.Conclusions
In summary, our data show that CHC is able to influence the intratumoral distribution of glucose use between hypoxic and non-hypoxic tumor areas. That is in accordance with a functional tumor lactate-shuttle, but the absence of any detectable changes in hypoxic extent and tissue metabolites was unexpected and warrants further investigation. 相似文献17.
The most lethal and debilitating attribute of cancer cells is their ability to metastasize. Throughout the process of metastasis, tumor cells interact with other tumor cells, host cells and a variety of molecules. Tumor cells are also faced with a number of insults, such as hemodynamic sheer pressure and immune selection. This brief review explores how metastasis suppressor proteins regulate interactions between tumor cells and the microenvironments in which tumor cells find themselves. 相似文献
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Zhongnan Yin Chunxiao Li Junjie Wang Lixiang Xue 《International journal of cancer. Journal international du cancer》2019,144(5):933-946
Cancer progression is closely related to the tumor microenvironment in which the tumor exists, including surrounding blood vessels, immune cells, fibroblasts, bone marrow-derived inflammatory cells, signaling molecules and the extracellular matrix. Tumors can influence the microenvironment by releasing extracellular signals, promoting tumor angiogenesis and inducing peripheral immune tolerance, while the immune cells in the microenvironment can impact the growth and evolution of cancerous cells. One of major cell components in the tumor microenvironment is myeloid-derived suppressor cells (MDSCs), which promote tumor growth and metastasis directly or indirectly by recognizing other immune cells, producing cytokines and exerting their immunosuppression functions. MDSCs have emerged as major regulators of immune responses in cancer and key targets for treating cancer. There are many limitations and side-effect in approaches of conventional cancer therapy, including radiotherapy. It has grown up to be a burgeoning field that a combination of radiotherapy and immunotherapy applied to cancer therapy. Therefore, it is fundamental to explore the immune mechanism in the process of cancer treatment. Here, we reviewed the recent progress of MDSCs in roles of the tumor microenvironment and tumor radiotherapy. 相似文献