scholarly journals Human adenovirus serotypes 4 and 11 show higher binding affinity and infectivity for endothelial and carcinoma cell lines than serotype 5

2003 ◽  
Vol 84 (3) ◽  
pp. 687-695 ◽  
Author(s):  
Lei-Qing Zhang ◽  
Ya-Fang Mei ◽  
Göran Wadell
Keyword(s):  
Breast Cancer ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Binding Affinity ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Human Cancer ◽  
Flow Cytometric Analysis ◽  
Carcinoma Cell Lines ◽  
Infected Cells

Adenoviruses are promising vectors for human cancer gene therapy. However, the extensively used adenoviruses serotypes 2 and 5 (Ad2 and Ad5) from species C have a major disadvantage in being highly prevalent; thus, most adults have an immunity against the two viruses. Furthermore, the expression of coxsackievirus and adenovirus receptors for Ad2 and Ad5 varies in different cells. This study aims to identify adenovirus serotypes with specific tropism for endothelial cells and epithelial tumour cells. Comparison of the binding affinities of Ad31, Ad11, Ad5, Ad37, Ad4 and Ad41, belonging to species A–F, respectively, to established cell lines of hepatoma (HepG2), breast cancer (CAMA and MG7), prostatic cancer (DU145 and LNCaP) and laryngeal cancer (Hep2), as well as to endothelial cells (HMEC), was carried out by flow cytometric analysis. Ad11 from species B showed markedly higher binding affinity than Ad5 for the endothelial cell line and all carcinoma cell lines studied. Ad4 showed a specific binding affinity for hepatoma cells and laryneal carcinoma cells. The ability of Ad11, Ad4 and Ad5 to be expressed in hepatoma, breast cancer and endothelial cell lines was studied by immunostaining and 35S-labelling of viral proteins in infected cells. Ad11 and Ad4 manifested a higher proportion of infected cells and a higher degree of hexon expression than Ad5.

scholarly journals ARA-Linker-TGFαL3: A Novel Chimera Protein to Target Breast Cancer Cells

2021 ◽  
Author(s):  
Abdolamir Ghadaksaz ◽  
Abbas Ali Imani Fooladi ◽  
Hamideh Mahmoodzadeh Hosseini ◽  
Taher Nejad Satari ◽  
Mohsen Amin
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Binding Affinity ◽  
Cell Lines ◽  
Cancer Cell ◽  
Recombinant Proteins ◽  
Breast Cancer Cells ◽  
Flow Cytometric Analysis ◽  
Breast Cancer Cell Lines

Abstract PurposeTargeted cancer therapies based on overexpressed receptors and the fractions containing immunotoxins and bacterial metabolites are one of the well-known methods to overcome the chemotherapy resistance of cancer cells. In this paper, we design ARA-linker-TGFαL3, using Arazyme, a Serratia proteamaculans metabolite, and a third loop segment of TGFα to target EGFR expressing breast cancer cells.MethodsAfter cloning in pET28a (+), the expression of recombinant protein was optimized in E. coli strain BL21 (DE3). MDA-MB-468 (EGFR positive) and MDA-MB-453 (EGFR negative) breast cancer cell lines were employed. Also, the chemotherapeutic drug, Taxotere (Docetaxel), was employed to compare cytotoxicity effects. Cell ELISA assessed the binding affinity of recombinant proteins to the receptor, and the cytotoxicity was detected by MTT and lactate dehydrogenase release assays. The interfacing with cancer cell adhesion was evaluated. Furthermore, the induction of apoptosis was examined by using flow cytometric analysis, and caspase-3 activity assay. Moreover, RT-PCR was conducted to study the expression of apoptosis (bax, bcl2, and casp3), angiogenesis (vegfr2), and metastasis (mmp2 and mmp9) genes. ResultsARA-linker-TGFαL3 revealed a higher binding affinity, cytotoxicity, and early apoptosis induction in MDA-MB-468 compared to the effects of Arazyme while both recombinant proteins showed similar effects on MDA-MB-453. In addition, the Taxotere caused the highest cytotoxicity on cancer cells through induction of late apoptosis. Meanwhile, the expression of angiogenesis and metastasis genes was decreased in both cell lines after treatment with either ARA-linker-TGFαL3 or Arazyme. ConclusionsOur in vitro results indicated the therapeutic effect of ARA-linker-TGFαL3 on breast cancer cells.

Productivein vitroinfection of human umbilical vein endothelial cells and three colon carcinoma cell lines with HIV-1

1995 ◽  
Vol 73 (2) ◽  
pp. 140-145 ◽  
Author(s):  
JACQUES CORBEIL ◽  
LOUISE A. EVANS ◽  
PAUL W. MCQUEEN ◽  
EVA VASAK ◽  
PAUL D. EDWARD ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Colon Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Carcinoma Cell Lines ◽  
Umbilical Vein Endothelial Cells ◽  
Hiv 1

scholarly journals The exostosin family of glycosyltransferases: mRNA expression profiles and heparan sulphate structure in human breast carcinoma cell lines

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Lawrence F. Sembajwe ◽  
Kirankumar Katta ◽  
Mona Grønning ◽  
Marion Kusche-Gullberg
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Breast Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Expression Profiles ◽  
Heparan Sulphate ◽  
Gene Expression Profiles ◽  
Carcinoma Cell Lines ◽  
Breast Carcinoma Cell Lines

Breast cancer remains a leading cause of cancer-related mortality in women. In recent years, regulation of genes involved in heparan sulphate (HS) biosynthesis have received increased interest as regulators of breast cancer cell adhesion and invasion. The exostosin (EXT) proteins are glycosyltransferases involved in elongation of HS, a regulator of intracellular signaling, cell–cell interactions, and tissue morphogenesis. The EXT family contains five members: EXT1, EXT2, and three EXT-like (EXTL) members: EXTL1, EXTL2, and EXTL3. While the expression levels of these enzymes change in tumor cells, little is known how this changes the structure and function of HS. In the present study, we investigated gene expression profiles of the EXT family members, their glycosyltransferase activities and HS structure in the estrogen receptor (ER), and progesterone receptor (PR) positive MCF7 cells, and the ER, PR, and human epidermal growth factor receptor-2 (HER2) negative MDA-MB-231 and HCC38 epithelial breast carcinoma cell lines. The gene expression profiles for MDA-MB-231 and HCC38 cells were very similar. In both cell lines EXTL2 was found to be up-regulated whereas EXT2 was down-regulated. Interestingly, despite having similar expression of HS elongation enzymes the two cell lines synthesized HS chains of significantly different lengths. Furthermore, both MDA-MB-231 and HCC38 exhibited markedly decreased levels of HS 6-O-sulphated disaccharides. Although the gene expression profiles of the elongation enzymes did not correlate with the length of HS chains, our results indicated specific differences in EXT enzyme levels and HS fine structure characteristic of the carcinogenic properties of the breast carcinoma cells.

scholarly journals Effect of Invasion of Borrelia burgdorferi in Normal and Neoplastic Mammary Epithelial Cells

Antibiotics ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1295
Author(s):  
Gauri Gaur ◽  
Janhavi Y. Sawant ◽  
Ankita S. Chavan ◽  
Vishwa A. Khatri ◽  
Yueh-Hsin Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Carcinoma ◽  
Epithelial Cells ◽  
Borrelia Burgdorferi ◽  
Cell Lines ◽  
Mammary Epithelial Cells ◽  
Carcinoma Cell ◽  
Mammary Epithelial ◽  
Carcinoma Cell Lines ◽  
Breast Carcinoma Cell Lines

Borrelia burgdorferi, the causative agent of Lyme Disease, is known to be able to disseminate and colonize various organs and tissues of its hosts, which is very crucial for its pathogenicity and survival. Recent studies have shown the presence of B. burgdorferi DNA in various breast cancer tissues, in some with poor prognosis, which raises the question about whether B. burgdorferi can interact with mammary epithelial cells and could have any effect on their physiology, including tumorigenic processes. As the model in this study, we have used MCF 10A normal and MDA-MB-231 tumorigenic mammary epithelial cells and infected both cell lines with B. burgdorferi. Our immunofluorescence and confocal microscopy results showed that B. burgdorferi is capable of invading normal epithelial and breast carcinoma cell lines within 24 h; however, the infection rate for the breast carcinoma cell lines was significantly higher. While the infection of epithelial cells with B. burgdorferi did not cause any changes in cell proliferation rates, it showed a significant effect on the invasion and migratory capacity of the breast cancer cells, but not on the normal epithelial cells, as determined by Matrigel invasion and wound healing assays. We have also found that the levels of expression of several epithelial–mesenchymal transition (EMT) markers (fibronectin, vimentin, and Twist1/2) changed, with a significant increase in tissue remodeling marker (MMP-9) in MDA-MB-231 cells demonstrated by quantitative Western blot analyses. This observation further confirmed that B. burgdorferi infection can affect the in vitro migratory and invasive properties of MDA-MB-231 tumorigenic mammary epithelial cells. In summary, our results suggest that B. burgdorferi can invade breast cancer tumor cells and it can increase their tumorigenic phenotype, which urges the need for further studies on whether B. burgdorferi could have any role in breast cancer development.

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