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Find video protocols related to scientific articles indexed in Pubmed.
Metformin enhances tamoxifen-mediated tumor growth inhibition in ER-positive breast carcinoma.
BMC Cancer
PUBLISHED: 03-05-2014
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Tamoxifen, an endocrine therapy drug used to treat breast cancer, is designed to interrupt estrogen signaling by blocking the estrogen receptor (ER). However, many ER-positive patients are low reactive or resistant to tamoxifen. Metformin is a widely used anti-diabetic drug with noteworthy anti-cancer effects. We investigated whether metformin has the additive effects with tamoxifen in ER-positive breast cancer therapy.
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Combination of SLC administration and tregs depletion is an attractive strategy for targeting hepatocellular carcinoma.
Mol. Cancer
PUBLISHED: 07-23-2013
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Secondary lymphoid tissue chemokine (SLC) is a key CC chemokine for chemotaxis of immune cells and has been an attractive candidate for anti-tumor treatments. However, among the immune cells recruited by SLC to tumors, the CD25+ Foxp3+ regulatory T cells (Tregs) compromise the anti-tumor effects. In this study, we proposed the combination therapy of intratumoral co-administration of SLC and anti-CD25 monoclonal antibodies (mAbs). We hypothesized that the intratumoral injections of SLC and depletion of Tregs would have stronger inhibition effects for the progression of hepatocellular carcinoma (HCC) in mice.
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CCR7 expression and intratumoral FOXP3+ regulatory T cells are correlated with overall survival and lymph node metastasis in gastric cancer.
PLoS ONE
PUBLISHED: 01-01-2013
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The aim of this study was to investigate the prognostic value of chemokine receptor CCR7 expression and intratumoral FOXP3(+) regulatory T cells (Tregs) in gastric cancer. CCR7(+) tumor cells and FOXP3(+) Tregs were assessed by immunohistochemistry in tissue microarrays containing gastric cancer from 133 patients. Prognostic effects of low or high CCR7 and FOXP3 expression were evaluated by Cox regression and Kaplan-Meier analysis, as well as the correlation between CCR7 positive score and intratumoral FOXP3(+) cell number in a longitudinal assessment. The analysis showed that the high expression levels of CCR7 and FOXP3 were detected in 69.9% and 65.4% of cases, respectively. High CCR7 expression in gastric cancer cells was significantly associated with poor overall survival (OS) (P = 0.010) and lymph node metastasis (P = 0.009), and was an independent factor for worse OS (P = 0.023) by multivariate analysis. High numbers of intratumoral FOXP3(+) Tregs significantly correlated with shorter OS (P = 0.021) and lymph node metastasis (P = 0.024), and was also an independent factor for adverse OS (P = 0.035). Furthermore, there was a significantly positive correlation between CCR7 positive score and intratumoral FOXP3(+) cell number (r = 0.949, P<0.001). These results revealed that CCR7 expression in gastric cancer cells and intratumoral FOXP3(+) Tregs could be considered as a co-indicator of clinical prognosis of gastric cancer.
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Depletion of CD4+ CD25+ regulatory T cells promotes CCL21-mediated antitumor immunity.
PLoS ONE
PUBLISHED: 01-01-2013
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CCL21 is known to attract dendritic cells (DCs) and T cells that may reverse tumor-mediated immune suppression. The massive infiltration of tumors by regulatory T cells (Tregs) prevents the development of a successful helper immune response. In this study, we investigated whether elimination of CD4(+) CD25(+) Tregs in the tumor microenvironment using anti-CD25 monoclonal antibodies (mAbs) was capable of enhancing CCL21-mediated antitumor immunity in a mouse hepatocellular carcinoma (HCC) model. We found that CCL21 in combination with anti-CD25 mAbs (PC61) resulted in improved antitumor efficacy and prolonged survival, not only inhibited tumor angiogenesis and cell proliferation, but also led to significant increases in the frequency of CD4(+), CD8(+) T cells and CD11c(+) DCs within the tumor, coincident with marked induction of tumor-specific CD8(+) cytotoxic T lymphocytes (CTLs) at the local tumor site. The intratumoral immune responses were accompanied by the enhanced elaboration of IL-12 and IFN-?, but reduced release of the immunosuppressive mediators IL-10 and TGF-?1. The results indicated that depletion of Tregs in the tumor microenvironment could enhance CCL21-mediated antitumor immunity, and CCL21 combined with anti-CD25 mAbs may be a more effective immunotherapy to promote tumor rejection.
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Role of activated rac1/cdc42 in mediating endothelial cell proliferation and tumor angiogenesis in breast cancer.
PLoS ONE
PUBLISHED: 01-01-2013
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Angiogenesis is a well-established target in anti-cancer therapy. Although vascular endothelial growth factor (VEGF)-mediated angiogenesis apparently requires the Rho GTPases Rac1 and Cdc42, the relevant mechanisms are unclear. Here, we determined that activated Rac1/Cdc42 in MCF-7 breast cancer cells could decrease p53 protein levels and increase VEGF secretion to promote proliferation and tube formation of human umbilical vein endothelial cells (HUVECs). However, these effects are reversed after ubiquitin-proteasome breakage. In exploring potential mechanisms for this relationship, we confirmed that activated Rac1/Cdc42 could enhance p53 protein ubiquitination and weaken p53 protein stability to increase VEGF expression. Furthermore, in a xenograft model using nude mice that stably express active Rac1/Cdc42 protein, active Rac1/Cdc42 decreased p53 levels and increased VEGF expression. Additionally, tumor angiogenesis was inhibited, and p53 protein levels were augmented, by intratumoral injection of the ubiquitin-proteasome inhibitor MG132. Finally in 339 human breast cancer tissues, our analyses indicated that Rac1/Cdc42 expression was related to advanced TNM staging, high proliferation index, ER status, and positive invasive features. In particular, our data suggests that high Rac1/Cdc42 expression is correlated with low wt-p53 and high VEGF expression. We conclude that activated Rac1/Cdc42 is a vascular regulator of tumor angiogenesis and that it may reduce stability of the p53 protein to promote VEGF expression by enhancing p53 protein ubiquitin.
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Up-regulation of Nob1 in the rat auditory system with noise-induced hearing loss.
Neurosci. Lett.
PUBLISHED: 01-04-2011
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The Nob1 gene is assumed to be associated with transcription regulation and may play important roles in mediating some physiological and pathological functions. Here, the rats were randomized equally into experimental group and control group. In experimental group, all subjects were exposed to 4-kHz octave-band noise at 110 dB SPL, 8 h per day for 7 days consecutively. Auditory thresholds were assessed by auditory brainstem response, prior to and 1 h after the cessation of noise exposure. Then, we investigated for the first time the expression of Nob1 in noise-exposed and noise-unexposed rats by quantitative polymerase chain reaction. The distribution of Nob1 in rat cochlea was further examined by immunohistochemistry. The results indicated that the hearing threshold was significantly higher in the noise-injured group than in the uninjured group after noise exposure. Nob1 mRNA was present at higher levels in regions of the noise-injured cochlea. As for noise-exposed rats, Nob1 expression was positive in the inner and outer hair cells of the organ of Corti and spiral ganglion neurons, but it undetectable in the uninjured cochlea. Therefore, Nob1 may play an important role in auditory function following acoustic trauma and can be used as a new target for the treatment of noise-induced hearing loss.
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Engineering injectable bone using bone marrow stromal cell aggregates.
Stem Cells Dev.
PUBLISHED: 12-29-2010
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With the increasing popularity of minimally invasive surgery, to develop an injectable bone would be highly preferable for the repair of bone nonunions and defects. However, the use of dissociated cells and exogenous carriers to construct injectable bone faces several drawbacks. To circumvent these limitations, we first harvested a cell sheet from rabbit bone marrow stromal cells using a continuous culture method and a scraping technique. The obtained sheet was then cut into fragments of multicellular aggregates, each of which was composed of a certain number of cells, extracellular matrix, and intercellular connections. The aggregates showed apparent mineralization properties, high alkaline phosphatase activity, increased osteocalcin content, and upregulated bone markers, implying their in vitro osteogenic potential. Then, serum-free medium (the control group), dissociated cell suspension (the cell group), and suspension of multicellular aggregates (the aggregate group) were injected subcutaneously on the back of the nude mice to evaluate ectopic bone formation. The results revealed that the aggregate group showed significantly larger and denser bone at the injection sites than the cell group, whereas bone formation did not occur in the control group. Additionally, when injecting them locally into the mandibular fracture gap of delayed healing in a rabbit model, we observed the most improved bone healing in the aggregate group. More cells survive and retain at the injection sites in the aggregate group than that in the cell group postoperatively. Our study indicates that the multicellular aggregates might be considered a promising strategy to generate injectable bone tissue and improve the efficacy of cell therapy.
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Higher intratumoral infiltrated Foxp3+ Treg numbers and Foxp3+/CD8+ ratio are associated with adverse prognosis in resectable gastric cancer.
J. Cancer Res. Clin. Oncol.
PUBLISHED: 02-01-2010
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The aim of the present study was to investigate the prognostic value of tumor-infiltrated lymphocytes (TILs), especially the prognostic value of Foxp3+ regulatory T cells (Tregs), CD8+ CTLs and Tregs/CD8+ ratios in gastric cancer patients after R0 resection.
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Effect of c-myc on the ultrastructural structure of cochleae in guinea pigs with noise induced hearing loss.
Biochem. Biophys. Res. Commun.
PUBLISHED: 09-19-2009
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Noise over-stimulation may induce hair cells loss and hearing deficit. The c-myc oncogene is a major regulator for cell proliferation, growth, and apoptosis. However, the role of this gene in the mammalian cochlea is still unclear. The study was designed to firstly investigate its function under noise condition, from the aspect of cochlear ultrastructural changes. We had established the adenoviral vector of c-myc gene and delivered the adenovirus suspension into the scala tympani of guinea pigs 4 days before noise exposure. The empty adenoviral vectors were injected as control. Then, all subjects were exposed to 4-kHz octave-band noise at 110dB SPL for 8h/day, 3 days consecutively. Auditory thresholds were assessed by auditory brainstem response, prior to and 7 days following noise exposure. On the seventh days after noise exposure, the cochlear sensory epithelia surface was observed microscopically and the cochleae were taken to study the ultrastructural changes. The results indicated that auditory threshold shift after noise exposure was higher in the ears treated with Ad.EGFP than that treated with Ad.c-myc-EGFP. Stereocilia loss and the disarrangement of outer hair cells were observed, with greater changes found in the Ad.EGFP group. Also, the ultrastructure changes were severe in the Ad.EGFP group, but not obvious in the Ad.c-myc-EGFP group. Therefore, c-myc gene might play an unexpected role in hearing functional and morphological protection from acoustic trauma.
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A comparison of the proliferative capacity and ultrastructure of proliferative cells from the cochleae of newborn rats of different ages.
Int. J. Pediatr. Otorhinolaryngol.
PUBLISHED: 07-18-2009
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Recent reports have shown that multipotent stem cells/progenitor cells that are capable of proliferation and regeneration are present in mammalian cochleae. However, progenitor cells have not been isolated from the adult cochlea. We examined the proliferative potential of cells derived from neonatal rats of various ages. The determination of the differences between the proliferative cells from rats of different ages may provide clues to the mechanisms controlling the destiny of these cells.
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The expression of NOB1 in spiral ganglion cells of guinea pig.
Int. J. Pediatr. Otorhinolaryngol.
PUBLISHED: 03-24-2009
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NOB1 was a transcription-associated protein, consisting of one zinc ribbon domain. This study aimed to investigate the NOB1 expression in spiral ganglion cells of normal guinea pigs and deaf ones.
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Overexpression of suppressor of cytokine signaling 1 in islet grafts results in anti-apoptotic effects and prolongs graft survival.
Life Sci.
PUBLISHED: 03-23-2009
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A significant portion of islet grafts are destroyed by apoptosis and fail to become functional after transplantation. Strategies that enhance islet resistance to apoptosis may prevent graft loss. The aim of this study was to investigate whether overexpression of suppressor of cytokine signaling 1 (SOCS1) in islet grafts could achieve an anti-apoptotic effect and prolong graft survival.
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Decreased level of cyclin A2 in rat cochlea development and cochlear stem cell differentiation.
Neurosci. Lett.
PUBLISHED: 02-09-2009
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Cyclin A2 plays a major role in cell cycle modulation. Cyclin A2 level has not been determined in the inner ear yet. RT-PCR, Western blotting, immunohistochemistry and immunocytochemistry were used to measure cyclin A2 expression in rat cochlea tissues of different ages, isolated cochlear stem cells and stem cell-derived differentiated cells. The results indicated that cyclin A2 level in cochlea tissues decreased gradually from newborn to adult. Furthermore, cyclin A2 level fell down after differentiation of cochlear stem cells. It was suggested that cyclin A2 might be involved in the modulation of rat cochlea development and cochlear stem cell differentiation.
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Establishing primary cultures of vascular smooth muscle cells from the spiral modiolar artery.
Int. J. Pediatr. Otorhinolaryngol.
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This article is reporting a method for establishment primary cultures of vascular smooth muscle cells (VSMCs) from the spiral modiolar artery (SMA).
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Identification of new altered genes in rat cochleae with noise-induced hearing loss.
Gene
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Because genes that are highly expressed in the cochlea after noise stress may have crucial regulatory roles in hearing, the identification of these genes may be useful for restoring normal auditory function. This study assessed altered gene expression at 1h following the cessation of noise exposure by using microarrays and real-time polymerase chain reaction (qPCR) in rats. In addition, the auditory threshold shifts and morphological changes of hair cells were observed. This study indicated that applied noise induced outer hair cell loss and a 40-50 dB hearing loss. Totally 239 altered genes were involved in the immune system process, response to stress, or response to stimulus. The expression of five up-regulated genes (Reg3b, Lcn2, Serpina3n, Nob1 and Hamp) was confirmed by qPCR. Future experiments will focus on several of these new candidate genes and may provide insight into the underlying auditory pathophysiology.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.