Influence of ALA-mediated photodynamic therapy on secretion of interleukins 6, 8 and 10 by colon cancer cells in vitro

2018 ◽  
Vol 22 ◽  
pp. 137-139 ◽  
Author(s):  
Aleksandra Kawczyk-Krupka ◽  
Zenon Czuba ◽  
Wojciech Latos ◽  
Katarzyna Wasilewska ◽  
Thomas Verwanger ◽  
...  
2019 ◽  
Vol 25 (1) ◽  
pp. 1-6 ◽  
Author(s):  
J. A. Rodrigues ◽  
R. Amorim ◽  
M. F. Silva ◽  
F. Baltazar ◽  
R. F. Wolffenbuttel ◽  
...  

Author(s):  
Aleksandra Kawczyk-Krupka ◽  
Marta Kaleta-Richter ◽  
Anna Miedzybrodzka ◽  
Wojciech Latos ◽  
Aleksander Sieron ◽  
...  

2020 ◽  
Vol 19 ◽  
pp. 153473542091893 ◽  
Author(s):  
Marta Kaleta-Richter ◽  
David Aebisher ◽  
Dagmara Jaworska ◽  
Zenon Czuba ◽  
Grzegorz Cieślar ◽  
...  

The aim of this study was to measure the secretion of interleukin (IL)-8 and -10 during an elicited immune response following sublethal doses of hypericin-mediated photodynamic therapy (HY-PDT) in experimental models of residual colon cancer cells in vitro. Investigations were performed on the cancer cell lines SW480 and SW620. Each cell line was exposed to 3 different concentrations of the photosensitizer HY and various doses of irradiation. The cell metabolic activity using an MTT assay was performed and then the measurement of IL-8 and IL-10 secretion was achieved using the Bio-Plex ProTMAssay. There was a statistically significant amplification of IL-8 secretion during HY-PDT in the SW620 cell line (at 1 J/cm2: P = .01, 5 J/cm2: P = .002, and 10 J/cm2: P = .025) and a statistically significant decrease in IL-8 during HY-PDT in the SW480 cell line (at 1 J/cm2: P = .05, 5 J/cm2: P = .035, and 10 J/cm2: P = .035). No statistically significant differences in IL-10 concentration were found following HY-PDT in the SW480 (at 1 J/cm2: P > .4, 5 J/cm2: P = .1, and 10 J/cm2: P = .075) or in the SW620 cell line (at 1 J/cm2: P > .4, 5 J/cm2: P > .4, and 10 J/cm2: P > .4). HY-PDT can both eliminate and control a primary tumor via cytotoxic effects, and at sublethal doses, it can affect IL release by colon cancer cells. In this experiment, this influence depended on the level of tumor cell metastatic activity.


2015 ◽  
Vol 12 (4) ◽  
pp. 598-611 ◽  
Author(s):  
Katarzyna Wawrzyniec ◽  
Aleksandra Kawczyk-Krupka ◽  
Zenon P. Czuba ◽  
Wojciech Król ◽  
Aleksander Sieroń

Author(s):  
Mayson H. Alkhatib ◽  
Dalal Al-Saedi ◽  
Wadiah S. Backer

The combination of anticancer drugs in nanoparticles has great potential as a promising strategy to maximize efficacies by eradicating resistant, reduce the dosage of the drug and minimize toxicities on the normal cells. Gemcitabine (GEM), a nucleoside analogue, and atorvastatin (ATV), a cholesterol lowering agent, have shown anticancer effect with some limitations. The objective of this in vitro study was to evaluate the antitumor activity of the combination therapy of GEM and ATVencapsulated in a microemulsion (ME) formulation in the HCT116 colon cancer cells. The cytotoxicity and efficacy of the formulation were assessed by the 3- (4,5dimethylthiazole-2-yl)-2,5-diphyneltetrazolium bromide (MTT) assay. The mechanism of cell death was examined by observing the morphological changes of treated cells under light microscope, identifying apoptosis by using the ApopNexin apoptosis detection kit, and viewing the morphological changes in the chromatin structure stained with 4′,6-diamidino-2-phenylindole (DAPI) under the inverted fluorescence microscope. It has been found that reducing the concentration of GEM loaded on ME (GEM-ME) from 5μM to 1.67μM by combining it with 3.33μM of ATV in a ME formulation (GEM/2ATV-ME) has preserved the strong cytotoxicity of GEM-ME against HCT116 cells. The current study proved that formulating GEM with ATV in ME has improved the therapeutic potential of GEM and ATV as anticancer drugs.


Author(s):  
Mattias Lepsenyi ◽  
Nader Algethami ◽  
Amr A. Al-Haidari ◽  
Anwar Algaber ◽  
Ingvar Syk ◽  
...  

AbstractPeritoneal metastasis is an insidious aspect of colorectal cancer. The aim of the present study was to define mechanisms regulating colon cancer cell adhesion and spread to peritoneal wounds after abdominal surgery. Mice was laparotomized and injected intraperitoneally with CT-26 colon carcinoma cells and metastatic noduli in the peritoneal cavity was quantified after treatment with a CXCR2 antagonist or integrin-αV-antibody. CT-26 cells expressed cell surface chemokine receptors CXCR2, CXCR3, CXCR4 and CXCR5. Stimulation with the CXCR2 ligand, CXCL2, dose-dependently increased proliferation and migration of CT-26 cells in vitro. The CXCR2 antagonist, SB225002, dose-dependently decreased CXCL2-induced proliferation and migration of colon cancer cells in vitro. Intraperitoneal administration of CT-26 colon cancer cells resulted in wide-spread growth of metastatic nodules at the peritoneal surface of laparotomized animals. Laparotomy increased gene expression of CXCL2 at the incisional line. Pretreatment with CXCR2 antagonist reduced metastatic nodules by 70%. Moreover, stimulation with CXCL2 increased CT-26 cell adhesion to extracellular matrix (ECM) proteins in a CXCR2-dependent manner. CT-26 cells expressed the αV, β1 and β3 integrin subunits and immunoneutralization of αV abolished CXCL2-triggered adhesion of CT-26 to vitronectin, fibronectin and fibrinogen. Finally, inhibition of the αV integrin significantly attenuated the number of carcinomatosis nodules by 69% in laparotomized mice. These results were validated by use of the human colon cancer cell line HT-29 in vitro. Our data show that colon cancer cell adhesion and growth on peritoneal wound sites is mediated by a CXCL2-CXCR2 signaling axis and αV integrin-dependent adhesion to ECM proteins.


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