scholarly journals The Impact of Melatonin on Colon Cancer Cells’ Resistance to Doxorubicin in an in Vitro Study

2017 ◽  
Vol 18 (7) ◽  
pp. 1396 ◽  
Author(s):  
Magdalena Fic ◽  
Agnieszka Gomulkiewicz ◽  
Jedrzej Grzegrzolka ◽  
Marzenna Podhorska-Okolow ◽  
Maciej Zabel ◽  
...  
2017 ◽  
Vol 12 (2) ◽  
pp. 196-200 ◽  
Author(s):  
Samira Rasouli Koohi ◽  
Mohammad Ali Derakhshan ◽  
Faramarz Faridani ◽  
Samad Muhammad Nejad ◽  
Saeid Amanpour ◽  
...  

Author(s):  
Mohd Adzim Khalili Rohin ◽  
Norhayati Abd Hadi ◽  
Norhaslinda Ridzwan

Aims: To examine the anti-proliferative properties of different extracts of new variety an organic rice MRQ74 towards colon cancer cells: in-vitro study. Study Design: Experimental study. Place and Duration of Study: Central Laboratory, Tissue Culture Laboratory, University of Sultan Zainal Abidin, Terengganu from November 2019 until February 2020. Methodology: The organic rice MRQ74 extracts had been led to tetrazolium salt reduction (MTT) assay and an inhibition concentration of 50 (IC50) value for their cytotoxic potential against colon cancer cells. Meanwhile, cells morphology observation and fluorescence double staining of treatment cells were determined using a light inverted microscope and acridine orange/propidium iodide staining. Results: Results showed that 50% aqueous ethanol of rice grains gave the lowest IC50 values towards HCT-116 and CT-26 cell lines, while an aqueous solution of rice grains gave the lowest IC50 values towards HT-29 cells (p<0.05). Thoroughly, the treated colon cancer cells had shown morphological alterations after treated with different solvent extracts of an organic rice MRQ74. Conclusion: The outcomes had observed preliminary results on cancer study for better health by inspiring the consumption of an organic rice MRQ74 and future product developments.


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.


2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 636-636 ◽  
Author(s):  
Dawei Li ◽  
Qingguo Li ◽  
Changhua Zhuo ◽  
Ye Xu ◽  
Sanjun Cai

636 Background: Distant metastasis remains the most common causes to death of colon cancer. Thus it is crucial to identify the molecular markers associated with the progression and metastasis of this disease. Recent evidence for overexpression of FOXC1 in several types of human cancer suggests that it might play a key role in tumor biology. However, the clinical significance of FOXC1 signaling in human colon cancer pathogenesis remains unknown. Methods: We investigated FOXC1 expression in 203 cases of primary colon cancer and matched normal colon tissue and lymph node matastasis in a tissue array. The underlying mechanisms of altered FOXC1 expression and the impact of this altered expression on colon cancer growth and metastasis was explored both in vitro and in vivo. Results: We found elevated expression of FOXC1 protein in cancereous tissue and lymph node metastases than adjacent normal colonic tissues. Overexpression of FOXC1 was associated with higher clinical stage, T stage, lymph node metastasis and presence of distant metastasis. FOXC1 served as an independent prognostic marker whose expression levels correlated with poorer metastasis-free survival (MFS) and poorer overall survival (OS). A Cox proportional hazards model revealed that FOXC1 expression was an independent prognostic factor in multivariate analysis. Experimentally, FOXC1 silencing significantly inhibited the growth and metastasis of colon cancer cells in vitro and in vivo. FOXC1 transcriptionally regulates SNAIL1, contributing to epithelial-to-mesenchymal transition and metastasis in colon cancer cells. Conclusions: Dysregulated expression of FOXC1 may play a critical role in colon cancer progression and metastasis. Thus, FOXC1 may serve as a candidate prognostic biomarker and therapeutically targeted.


Cancers ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 366
Author(s):  
Gaëtan Mary ◽  
Brice Malgras ◽  
Jose Efrain Perez ◽  
Irène Nagle ◽  
Nathalie Luciani ◽  
...  

A growing tumor is submitted to ever-evolving mechanical stress. Endoscopic procedures add additional constraints. However, the impact of mechanical forces on cancer progression is still debated. Herein, a set of magnetic methods is proposed to form tumor spheroids and to subject them to remote deformation, mimicking stent-imposed compression. Upon application of a permanent magnet, the magnetic tumor spheroids (formed from colon cancer cells or from glioblastoma cells) are compressed by 50% of their initial diameters. Such significant deformation triggers an increase in the spheroid proliferation for both cell lines, correlated with an increase in the number of proliferating cells toward its center and associated with an overexpression of the matrix metalloproteinase−9 (MMP−9). In vivo peritoneal injection of the spheroids made from colon cancer cells confirmed the increased aggressiveness of the compressed spheroids, with almost a doubling of the peritoneal cancer index (PCI), as compared with non-stimulated spheroids. Moreover, liver metastasis of labeled cells was observed only in animals grafted with stimulated spheroids. Altogether, these results demonstrate that a large compression of tumor spheroids enhances cancer proliferation and metastatic process and could have implications in clinical procedures where tumor compression plays a role.


2017 ◽  
Vol 7 ◽  
pp. 1-8 ◽  
Author(s):  
Senthiladipan Venkatachalam ◽  
Esther Mettler ◽  
Christian Fottner ◽  
Matthias Miederer ◽  
Bernd Kaina ◽  
...  

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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