A Novel In Vitro Model of Lymphatic Metastasis from Colorectal Cancer

2007 ◽  
Vol 143 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Peter S. Yoo ◽  
Abby L. Mulkeen ◽  
Alan Dardik ◽  
Charles H. Cha
Keyword(s):  
Colorectal Cancer ◽  
Lymphatic Metastasis ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Efficacy of DOPE/DC-cholesterol liposomes and GCPQ micelles as AZD6244 nanocarriers in a 3D colorectal cancer in vitro model

Nanomedicine ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. 331-344 ◽  
Author(s):  
Víctor López-Dávila ◽  
Tarig Magdeldin ◽  
Hazel Welch ◽  
Miriam Victoria Dwek ◽  
Ijeoma Uchegbu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals The efficacy of cetuximab in a tissue-engineered three-dimensional in vitro model of colorectal cancer

2014 ◽  
Vol 5 ◽  
pp. 204173141454418 ◽  
Author(s):  
Tarig Magdeldin ◽  
Víctor López-Dávila ◽  
Cecile Villemant ◽  
Grant Cameron ◽  
Rosemary Drake ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
In Vitro Model ◽  
Three Dimensional ◽  
Vitro Model

scholarly journals A new in vitro model applied 90Y microspheres to study the effects of low dose beta radiation on colorectal cancer cell line in various oxygenation conditions

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Piotr Piasecki ◽  
Aleksandra Majewska ◽  
Jerzy Narloch ◽  
Maciej Maciak ◽  
Klaudia Brodaczewska ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
In Vitro Model ◽  
Absorbed Dose ◽  
Cancer Cell Line ◽  
Colorectal Cancer Cell ◽  
Beta Radiation ◽  
Colorectal Cancer Cell Line ◽  
Vitro Model

AbstractWe propose a new in vitro model to assess the impact of 90Y-microspheres derived low-dose beta radiation on colorectal cancer cell line under various oxygenation conditions that mimic the tumor environment. Cancer cells (HCT116) proliferation was assessed using Alamar Blue (AB) assay after 48, 72, and 96 h. FLUKA code assessed changes in cancer cell populations relative to the absorbed dose. In normoxia, mitochondrial activity measured by Alamar Blue after 48–72 h was significantly correlated with the number of microspheres (48 h: r = 0.87 and 72 h: r = 0.89, p < 0.05) and absorbed dose (48 h: r = 0.87 and 72 h: r = 0.7, p < 0.05). In hypoxia, the coefficients were r = 0.43 for both the number of spheres and absorbed dose and r = 0.45, r = 0.47, respectively. Impediment of cancer cell proliferation depended on the absorbed dose. Doses below 70 Gy could reduce colorectal cancer cell proliferation in vitro. Hypoxia induced a higher resistance to radiation than that observed under normoxic conditions. Hypoxia and radiation induced senescence in cultured cells. The new in vitro model is useful for the assessment of 90Y radioembolization effects at the micro-scale.

scholarly journals Short-term spheroid culture of primary colorectal cancer cells as an in vitro model for personalizing cancer medicine

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0183074 ◽  
Author(s):  
Maria Jeppesen ◽  
Grith Hagel ◽  
Anders Glenthoj ◽  
Ben Vainer ◽  
Per Ibsen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
In Vitro Model ◽  
Primary Colorectal Cancer ◽  
Short Term ◽  
Spheroid Culture ◽  
Colorectal Cancer Cells ◽  
Cancer Medicine ◽  
Vitro Model

scholarly journals Endothelin-1 as a Mediator of Heme Oxygenase-1-Induced Stemness in Colorectal Cancer: Influence of p53

2021 ◽  
Vol 11 (6) ◽  
pp. 509
Author(s):  
Sandra Ríos-Arrabal ◽  
Jose D. Puentes-Pardo ◽  
Sara Moreno-SanJuan ◽  
Ágata Szuba ◽  
Jorge Casado ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Heme Oxygenase ◽  
In Vitro Model ◽  
Cell Model ◽  
Heme Oxygenase 1 ◽  
Wild Type ◽  
Endothelin 1 ◽  
Endothelin Converting Enzyme ◽  
Vitro Model

Heme oxygenase-1 (HO-1) is an antioxidant protein implicated in tumor progression, metastasis, and resistance to therapy. Elevated HO-1 expression is associated with stemness in several types of cancer, although this aspect has not yet been studied in colorectal cancer (CRC). Using an in vitro model, we demonstrated that HO-1 overexpression regulates stemness and resistance to 5-FU treatment, regardless of p53. In samples from CRC patients, HO-1 and endothelin converting enzyme-1 (ECE-1) expression correlated significantly, and p53 had no influence on this result. Carbon monoxide (CO) activated the ECE-1/endothelin-1 (ET-1) pathway, which could account for the protumoral effects of HO-1 in p53 wild-type cells, as demonstrated after treatment with bosentan (an antagonist of both ETRA and ETRB endothelin-1 receptors). Surprisingly, in cells with a non-active p53 or a mutated p53 with gain-of-function, ECE-1-produced ET-1 acted as a protective molecule, since treatment with bosentan led to increased efficiency for spheres formation and percentage of cancer stem cells (CSCs) markers. In these cells, HO-1 could activate or inactivate certain unknown routes that could induce these contrary responses after treatment with bosentan in our cell model. However more research is warranted to confirm these results. Patients carrying tumors with a high expression of both HO-1 and ECE-1 and a non-wild-type p53 should be considered for HO-1 based-therapies instead of ET-1 antagonists-based ones.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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