scholarly journals Jacalin-Activated Macrophages Exhibit an Antitumor Phenotype

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Cláudia Danella Polli ◽  
Luciana Pereira Ruas ◽  
Luciana Chain Veronez ◽  
Thais Herrero Geraldino ◽  
Fabiana Rossetto de Morais ◽  
...  

Tumor-associated macrophages (TAMs) have an ambiguous and complex role in the carcinogenic process, since these cells can be polarized into different phenotypes (proinflammatory, antitumor cells or anti-inflammatory, protumor cells) by the tumor microenvironment. Given that the interactions between tumor cells and TAMs involve several players, a better understanding of the function and regulation of TAMs is crucial to interfere with their differentiation in attempts to skew TAM polarization into cells with a proinflammatory antitumor phenotype. In this study, we investigated the modulation of macrophage tumoricidal activities by the lectin jacalin. Jacalin bound to macrophage surface and induced the expression and/or release of mainly proinflammatory cytokines via NF-κB signaling, as well as increased iNOS mRNA expression, suggesting that the lectin polarizes macrophages toward the antitumor phenotype. Therefore, tumoricidal activities of jacalin-stimulated macrophages were evaluated. High rates of tumor cell (human colon, HT-29, and breast, MCF-7, cells) apoptosis were observed upon incubation with supernatants from jacalin-stimulated macrophages. Taken together, these results indicate that jacalin, by exerting a proinflammatory activity, can direct macrophages to an antitumor phenotype. Deep knowledge of the regulation of TAM functions is essential for the development of innovative anticancer strategies.

2019 ◽  
Vol 74 (1) ◽  
pp. 107-114 ◽  
Author(s):  
Ana Clara Sabbione ◽  
Fredrick Onyango Ogutu ◽  
Adriana Scilingo ◽  
Miao Zhang ◽  
María Cristina Añón ◽  
...  

1985 ◽  
Vol 122 (1) ◽  
pp. 21-29 ◽  
Author(s):  
Alain Zweibaum ◽  
Mo�se Pinto ◽  
Guillemette Chevalier ◽  
Elisabeth Dussaulx ◽  
Nicole Triadou ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Erhui Jiang ◽  
Tinglin Yan ◽  
Zhi Xu ◽  
Zhengjun Shang

Cell fusion is a highly regulated biological process that occurs under both physiological and pathological conditions. The cellular and extracellular environment is critical for the induction of the cell–cell fusion. Aberrant cell fusion is initiated during tumor progression. Tumor microenvironment is a complex dynamic system formed by the interaction between tumor cells and their surrounding cells. Cell–cell fusion mediates direct interaction between tumor cells and their surrounding cells and is associated with tumor initiation and progression. Various microenvironmental factors affect cell fusion in tumor microenvironment and generate hybrids that acquire genomes of both parental cells and exhibit novel characteristics, such as tumor stem cell-like properties, radioresistance, drug resistance, immune evasion, and enhanced migration and invasion abilities, which are closely related to the initiation, invasion, and metastasis of tumor. The phenotypic characteristics of hybrids are based on the phenotypes of parental cells, and the fusion of tumor cells with diverse types of microenvironmental fusogenic cells is concomitant with phenotypic heterogeneity. This review highlights the types of fusogenic cells in tumor microenvironment that can fuse with tumor cells and their specific significance and summarizes the various microenvironmental factors affecting tumor cell fusion. This review may be used as a reference to develop strategies for future research on tumor cell fusion and the exploration of cell fusion-based antitumor therapies.


2017 ◽  
Vol 12 (5) ◽  
pp. 1934578X1701200
Author(s):  
Rosa Martí-Centelles ◽  
Juan Murga ◽  
Eva Falomir ◽  
Miguel Carda ◽  
J. Alberto Marco

A group of 28 N-benzylidene aniline derivatives structurally related to the natural stilbene resveratrol has been prepared through condensation of anilines with the corresponding aldehydes. The ability of these imines to inhibit proliferation of two tumor cell lines (HT-29 and MCF-7) and one non-tumor cell line (HEK-293) was first determined. Subsequently, we determined the ability of some of the most cytotoxic compounds to inhibit the secretion of the VEGF-A factor in HT-29 cells and to downregulate the expression of the VEGF and hTERT genes, the latter one being involved in the activation of telomerase.


Author(s):  
Jesica M. Ramírez-Villalobos ◽  
César I. Romo-Sáenz ◽  
Karla S. Morán-Santibañez ◽  
Patricia Tamez-Guerra ◽  
Ramiro Quintanilla-Licea ◽  
...  

Endophytic fungi have become potential sources of antitumor agents, particularly against antineoplastic-resistant cancer cells, with marginal or nil adverse effects for the oncological patient. Endophytic fungi were isolated from stems of the Lophocereus marginatus cactus, commonly found in Mexico. Methanol extracts were then obtained from fungus liquid cultures and their effects on tumor cell growth against murine lymphoma (L5178Y-R), human colorectal adenocarcinoma (HT-29), and human breast cancer (MCF-7) cells were evaluated at concentrations ranging from 31 µg/mL to 250 µg/mL via the colorimetric 3- [4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazoliumbromide reduction assay, using monkey kidney epithelial (MA-104) and human peripheral mononuclear (PBMC) cells as controls. Furthermore, we obtained the IC50 and the selectivity index (SI) was calculated from the IC50 ratio of normal and tumor cells. In addition, molecular identification of fungi showing cytotoxic activity was determined, using internal transcribed spacer molecular markers. PME-H001, PME-H002, PME-H005, PME-H007, and PME-H008 filamentous fungus strain extracts showed significant (p < 0.05) tumor cell growth inhibition. In particular, they significantly (p < 0.05) inhibited L5178Y-R cell growth, whereas the least susceptible cell line was HT-29. The endophytic strain PME-H008 of Cladosporium sp. caused the highest growth inhibition percentage against L5178Y-R and HT-29 cells with 96.6% (p < 0.01) and 42.5% (p < 0.05) respectively, and the highest SIs against L5178Y-R cells with 2.4 and 2.9 for MA-104 and PBMCs, respectively, whereas the PME-H005 extract showed SIs of 2.77 and 1.5 against MCF-7 and L5178Y-R cells, respectively, as compared with PBMCs. In addition, the endophytic strain PME-H007 of Metarhizium anisopliae caused the highest percentage of growth inhibition (p < 0.01) against MCF-7 cells with 55.8% at 250 µg/mL. We demonstrated in vitro antitumor effects of L. marginatus endophytic fungi. Further research will involve the isolation and in vivo testing of bioactive compounds.


2020 ◽  
Author(s):  
Chenchen Huang ◽  
Fangrui Liu ◽  
Qiang Feng ◽  
Xinyan Pan ◽  
Shuling Song ◽  
...  

Abstract BackgroundAn anti-p21Ras scFv can specifically bind with mutant and wild-type p21Ras but cannot penetrate the cell membrane, which prevents it from binding to p21Ras in the cytoplasm. Here, the RGD4C peptide was used to mediate scFv penetration into tumor cells and produce an inhibitory effect.MethodsRGD4C-linker-EGFP and RGD4C-p21Ras-scFv recombinant expression plasmids were constructed, and the fusion proteins were expressed in E. coli and purified with HisPur Ni-NTA. RGD4C-linker-EFGP was used to test the factors affecting RGD4C penetration of the tumor cell membrane. The immunoreactivity of RGD4C-p21Ras-scFv toward p21Ras was identified by ELISA and western blotting. Moreover, immunocytochemistry was used to detect the ability of RGD4C-p21Ras-scFv to penetrate SW480 cells. Cell migration, colony formation, cell killing, and apoptosis assays were used to assess the inhibitory effect of RGD4C-p21Ras-scFv on SW480 cells in vitro.ResultsThe RGD4C peptide could target tumor cells, but endocytosis inhibitors and a low temperature inhibited RGD4C peptide endocytosis into cells, and tumor cell entry was time and concentration dependent. Additionally, a change in the cell membrane potential did not affect penetrability. We found that RGD4C-p21Ras-scFv could penetrate SW480 cells; effectively inhibit the growth, proliferation and migration of SW480 cells; and promote apoptosis in SW480 cells. ConclusionThe RGD4C peptide can mediate anti-p21Ras scFv entry into SW480 cells and produce an inhibitory effect, which indicates that RGD4C-p21Ras-scFv may be a potential therapeutic antibody for the treatment of RAS-mutant colorectal cancer.


1986 ◽  
Vol 488 (1 Membrane Path) ◽  
pp. 579-581 ◽  
Author(s):  
G. ESPOSITO ◽  
E. BOMBARDIERI ◽  
M. G. COCCIOLO ◽  
C. LINDI ◽  
M. VALTOLINA ◽  
...  

2021 ◽  
Vol 11 ◽  
Author(s):  
Yang Liu ◽  
Ke Shi ◽  
Yong Chen ◽  
Xianrui Wu ◽  
Zheng Chen ◽  
...  

Exosomes from extracellular vesicles can activate or inhibit various signaling pathways by transporting proteins, lipids, nucleic acids and other substances to recipient cells. In addition, exosomes are considered to be involved in the development and progression of tumors from different tissue sources in numerous ways, including remodeling of the tumor microenvironment, promoting angiogenesis, metastasis, and invasion, and regulating the immune escape of tumor cells. However, the precise molecular mechanisms by which exosomes participate in these different processes remains unclear. In this review, we describe the research progress of tumor cell-derived exosomes in cancer progression. We also discuss the prospects of the application of exosomes combined with nanoengineered chemotherapeutic drugs in the treatment of cancer.


1999 ◽  
Vol 27 (02) ◽  
pp. 265-275 ◽  
Author(s):  
J.G. Lin ◽  
J.G. Chung ◽  
L.T. Wu ◽  
G.W. Chen ◽  
H.L. Chang ◽  
...  

Berberine was used to determine loss of viable cells and inhibition of arylamine Nacetyltransferase (NAT) activity in a human colon tumor (adenocarcinoma) cell line. The viable cells were determined by trypan blue exclusion under a light microscope. The NAT activity was measured by high performance liquid chromatography for the amounts of N-acetyl-2-minofluorene (AAF), N-acetyl-p-aminobenzoic acid (N-Ac-PABA), and the remaining 2-aminofluorene (AF) and p-aminobenzoic acid (PABA). The viability and NAT activity in a human colon tumor cell line was inhibited by berberine in a dose-dependent manner, i.e., the higher the concentration of berberine, the higher the inhibition of NAT activity and cell death. The NAT activities measured in the intact human colon tumor cells were decreased over 50% by AAF and NAc-PABA production from acetylation of AF and PABA. The apparent values of Km and Vmax of NAT from colon tumor cells were also inhibited by berberine in cytosols and in intact cells. This report is the first to show that berberine did affect human colon tumor cell NAT activity.


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