scholarly journals Bioreducible PEI-siRNA Nanocomplex for Liver Cancer Therapy: Transfection, Biodistribution, and Tumor Growth InhibitionIn Vivo

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Xia ◽  
Yan Li ◽  
Bo Lou ◽  
Peijun Wang ◽  
Xiaolong Gao ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Tumor Growth ◽  
Plasmid Dna ◽  
Gold Standard ◽  
Hepg2 Cells ◽  
Cancer Gene Therapy ◽  
Nonviral Gene Delivery ◽  
Surface Charges

A bioreducible polyethylenimine (SS-PEI) was successfully applied as a nonviral carrier for the delivery of plasmid DNA and VEGF-siRNAin vitroandin vivo. The SS-PEI could strongly condense DNA or siRNA into nanosized complexes (below 200 nm) with positive surface charges.In vitrotransfection experiments using GFP plasmid as gene reporter showed that the complexes of SS-PEI/DNA were able to efficiently transfect HepG2 cells, with efficiency comparable to that of polyethylenimine, a gold standard for nonviral gene delivery. Moreover, the complexes of SS-PEI/VEGF-siRNA could lead to reduced levels of VEGF protein in HepG2 cellsin vitro. Treatment with the complexes of SS-PEI/VEGF-siRNA efficiently inhibited HepG2 tumor growth in an xenograft mouse model. The data of this study imply that the SS-PEI is a potent nucleic acid carrier applicable for liver cancer gene therapy.

Sodium 3-mercaptopropanesulphonate substituted phthalocyanine: Synthesis, photophysical properties, in vitro and in vivo PDT efficacy

2020 ◽  
pp. A-E
Author(s):  
Mack Biyiklioglu
Keyword(s):  
Tumor Growth ◽  
Singlet Oxygen ◽  
Hepg2 Cells ◽  
Photophysical Properties ◽  
Clinical Applications ◽  
In Vivo Studies ◽  
Cremophor El ◽  
Photochemical Properties

A new sulfonic zinc(II) phthalocyanine bearing sodium 3-mercaptopropanesulphonate (Pc) was synthesized and characterized, as to its photophysical and photochemical properties, in vitro and in vivo. Pc remain non-aggregated in [Formula: see text],[Formula: see text]-dimethylformamide and in water containing 0.1% Cremophor EL, with high singlet oxygen efficacy. In vitro studies showed that the IC[Formula: see text] value of Pc on HepG2 cells was 1.3 [Formula: see text]M. In addition, in vivo studies showed that Pc mainly accumulated in tumor sites and showed an obvious PDT effect, and ca.97% of tumor growth was inhibited. Therefore, the Pc could be applied as a very promising photosensitizer for PDT in future clinical applications.

scholarly journals Morphine Suppresses Liver Cancer Cell Tumor Properties In Vitro and In Vivo

2021 ◽  
Vol 11 ◽  
Author(s):  
Hao-Wen Zhang ◽  
Fei Wang ◽  
Ya-Qun Zhou ◽  
San-Ping Xu ◽  
Shi-Ying Yu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Hepg2 Cells ◽  
Cell Tumor ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
Sphere Formation

Morphine is an analgesic widely adopted to relieve cancer pain. A number of discrepancies, however, are presented by the published literature, with reports suggesting that opioids may either promote or inhibit the spread of cancer. It is of great significance to determine whether morphine may increase the risk of metastasis while utilized in liver cancer surgical treatment. In this study, we explore the effects of morphine on liver cancer cells in vitro and in vivo. Our results showed that morphine does not promote proliferative ability to cultured liver cancer cells. While morphine could increase the apoptosis rate of Hep3B/HepG2 cells. Furthermore, morphine could significantly inhibit the migratory and invasion ability of Hep3B/HepG2 cells. Subsequent investigations disclosed that morphine could inhibit sphere formation ability of Hep3B/HepG2 cells by using sphere formation assay. Based on nude mouse models, we demonstrated that morphine significantly reduced pulmonary tumorigenicity of Hep3B/HepG2 cells. In conclusion, our results found that morphine at clinical concentrations could suppress liver cancer cell tumor properties in vitro and in vivo, indicating the safety of morphine utilization in HCC patients’ pain management.

Melatonin Differentially Modulates NF-кB Expression in Breast and Liver Cancer Cells

2019 ◽  
Vol 18 (12) ◽  
pp. 1688-1694 ◽  
Author(s):  
Jucimara Colombo ◽  
Bruna V. Jardim-Perassi ◽  
João P.S. Ferreira ◽  
Cristine Z. Braga ◽  
Nathália M. Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Transcription Factor ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
In Vitro Study ◽  
Inhibitory Effect

Background: NF-kB (nuclear factor kappa B) is a transcription factor composed of two subunits, p50 and p65, which plays a key role in the inflammatory process. Melatonin has oncostatic, antiangiogenic and antimetastatic properties, and some recent studies have indicated an inhibitory effect of melatonin on NF-kB in some types of cancer. This work aims to investigate the effects of melatonin treatment on the expression of NFkB in breast and liver cancer models. Method: The breast cancer xenographic model was performed using female Balb/c nude athymic mice injected with MDA-MB-231 cells. The animals were treated with 40 mg/Kg of melatonin for 21 days. Volume of the tumors was measured with a digital caliper. Hepatocarcinoma model was developed by using the HepG2 cells in vitro, treated with 1 mM melatonin for 24 h. The expression of NF-kB protein was verified by immunohistochemistry and immunocytochemistry and quantified by optical densitometry, in vivo study and in vitro study, respectively. NF-kB gene expression was performed by quantitative RT-PCR. Results: The breast cancer xenografts nude mice treated with melatonin showed reduced tumor size (P=0.0022). There was a decrease in NF-kB protein staining (P=0.0027) and gene expression (P=0.0185) in mice treated with melatonin. The opposite results were observed for the hepatocarcinoma model. HepG2 cells treated with melatonin showed an increase in the NF-kB immunostaining when compared to control cells (P=0.0042). Conclusion: Our results indicated that the treatment with melatonin was able to decrease both gene and protein expressions of NF-kB in breast cancer cells and, conversely, increase the transcription factor protein expression in hepatocarcinoma cells. These data highlighted a double role in the expression of NF-kB, depending on the cell type. Further studies are needed to better elucidate the action of melatonin in NF-kB, since this transcription factor acts on different signaling pathways that are fundamental for carcinogenesis.

scholarly journals Expression and clinical significance of HMGB1 in human liver cancer: Knockdown inhibits tumor growth and metastasis in vitro and in vivo

2012 ◽  
Vol 29 (1) ◽  
pp. 87-94 ◽  
Author(s):  
YA-DONG DONG ◽  
LONG CUI ◽  
CHENG-HONG PENG ◽  
DONG-FENG CHENG ◽  
BAO-SAN HAN ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Tumor Growth ◽  
Clinical Significance ◽  
Human Liver ◽  
Human Liver Cancer ◽  
Tumor Growth And Metastasis

Melatonin modifies tumor hypoxia and metabolism by inhibiting HIF-1α and energy metabolic pathway in the in vitro and in vivo models of breast cancer

2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Carbonic Anhydrases ◽  
In Vivo Models ◽  
Ca Ix ◽  
Gene And Protein Expression

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 

Reprogrammed M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 extends lifespan of mice with experimental carcinoma

2017 ◽  
pp. 4-9
Author(s):  
С.В. Калиш ◽  
С.В. Лямина ◽  
А.А. Раецкая ◽  
И.Ю. Малышев
Keyword(s):  
Tumor Growth ◽  
Culture Medium ◽  
Ehrlich Carcinoma ◽  
Macrophage Phenotype ◽  
M1 Macrophages ◽  
M1 Macrophage ◽  
Ec Cells ◽  
Experimental Carcinoma

Цель исследования. Репрограммирование М1 фенотипа макрофагов с ингибированными факторами транскрипции М2 фенотипа STAT3, STAТ6 и SMAD и оценка их влияния на развитие карциномы Эрлиха (КЭ) in vitro и in vivo. Методика. Рост опухоли иницировали in vitro путем добавления клеток КЭ в среду культивирования RPMI-1640 и in vivo путем внутрибрюшинной инъекции клеток КЭ мышам. Результаты. Установлено, что M1макрофаги и in vitro, и in vivo оказывают выраженный противоопухолевый эффект, который превосходит антиопухолевые эффекты М1, M1, M1 макрофагов и цисплатина. Заключение. М1 макрофаги с ингибированными STAT3, STAT6 и/или SMAD3 эффективно ограничивают рост опухоли. Полученные данные обосновывают разработку новой технологии противоопухолевой клеточной терапии. Objective. Reprogramming of M1 macrophage phenotype with inhibited M2 phenotype transcription factors, such as STAT3, STAT6 and SMAD and assess their impact on the development of Ehrlich carcinoma (EC) in vitro and in vivo . Methods. Tumor growth in vitro was initiated by addition of EC cells in RPMI-1640 culture medium and in vivo by intraperitoneal of EC cell injection into mice. Results. It was found that M1 macrophages have a pronounced anti-tumor effect in vitro , and in vivo , which was greater than anti-tumor effects of M1, M1, M1 macrophages and cisplatin. Conclusion. M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.

The Inhibition Effect of Caveolin-1 on PANC1 Human Pancreatic Tumor Growth In vitro and In vivo*

2012 ◽  
Vol 38 (12) ◽  
pp. 1121-1131
Author(s):  
Xiao-Hui WANG ◽  
Ya-Min ZHENG ◽  
Ye-Qing CUI ◽  
Shuang LIU ◽  
Hai-Chen SUN ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Pancreatic Tumor ◽  
Caveolin 1 ◽  
Inhibition Effect

ANTITUMOR EFFECT OF COLLOIDAL SILVER BISILICATE IN EXPERIMENTAL IN VITRO AND IN VIVO STUDIES

2019 ◽  
Vol 65 (5) ◽  
pp. 760-765
Author(s):  
Margarita Tyndyk ◽  
Irina Popovich ◽  
A. Malek ◽  
R. Samsonov ◽  
N. Germanov ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Human Tumor ◽  
Significant Inhibition ◽  
In Vivo Studies ◽  
Ehrlich Carcinoma ◽  
In Vivo Experiments

The paper presents the results of the research on the antitumor activity of a new drug - atomic clusters of silver (ACS), the colloidal solution of nanostructured silver bisilicate Ag6Si2O7 with particles size of 1-2 nm in deionized water. In vitro studies to evaluate the effect of various ACS concentrations in human tumor cells cultures (breast cancer, colon carcinoma and prostate cancer) were conducted. The highest antitumor activity of ACS was observed in dilutions from 2.7 mg/l to 5.1 mg/l, resulting in the death of tumor cells in all studied cell cultures. In vivo experiments on transplanted Ehrlich carcinoma model in mice consuming 0.75 mg/kg ACS with drinking water revealed significant inhibition of tumor growth since the 14th day of experiment (maximally by 52% on the 28th day, p < 0.05) in comparison with control. Subcutaneous injections of 2.5 mg/kg ACS inhibited Ehrlich's tumor growth on the 7th and 10th days of the experiment (p < 0.05) as compared to control.

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