Colon cancer stem cells – From basic to clinical application

Botchkina, Galina I.

doi:10.1016/j.canlet.2012.04.006

Cited by 57 publications

(45 citation statements)

References 205 publications

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“…Thus, CSCs are an essential therapeutic target; however, conventional anticancer therapies are not effective in hindering CSCs [38,39] . We inhibited EA-induced metastasis by treatment with inhibition of the Wnt signal and ERK1/2, which suggests that EA-associated stemness might be enhanced through the MAPK-Wnt pathway.…”

Section: Discussionmentioning

confidence: 99%

Elaidic Acid, a Trans-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells

et al. 2016

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The effects of trans-fatty acids (TFAs) on cardiovascular disorders have been extensively studied, and the effect of TFAs on cancers has recently been recognized. This study examined the effects of elaidic acid (EA), a TFA, on colorectal cancer (CRC) progression. We demonstrated that EA enhanced the growth, survival, and invasion of the CRC cell lines, CT26, and HT29. Tumor growth and metastasis in the lung, liver, and peritoneum were significantly more enhanced in CRC cells treated with EA than those treated with the cis form of EA, oleic acid (OA), or vehicle. Spheres of CRC cells were formed at more pronounced numbers in EA-treated cells than in OA-treated cells. Compared to OA, EA treatment also induced expression of the stemness factors, nucleostemin, CD133, and Oct4. Moreover, spheres of EA-treated CRC cells were larger and more proliferative than spheres of OA-treated cells. Oral intake of EA also enhanced liver metastasis and CD133 expression of CRC cells in a dose-dependent manner. EA intake also increased resistance to 5-fluorouracil. Inhibition of Wnt and ERK1/2 abrogated EA-induced enhancement of metastasis. Our findings demonstrate that EA might provide prominent metastatic potential to CRC cells, which shows important implications for the treatment of CRC.

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Section: Discussionmentioning

confidence: 99%

Elaidic Acid, a Trans-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells

et al. 2016

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“…b Rate of c-kit internalization upon protein binding due to receptor-mediated endocytosis was indirectly measured by staining surface c-kit with anti-CD117 PE antibody. Decrease in the relative MFI upon binding of each protein to the three cell lines obtained from flow cytometric analysis was plotted in terms of a graph using GraphPad software antibody dilution used (Botchkina 2013;Miettinen and Lasota 2005;Sabah et al 2003). Accordingly, we identified NBs and CRCs expressing SCF/c-kit autocrine growth loops as the target niche for in vitro protein characterization.…”

Section: Discussionmentioning

confidence: 99%

Targeting c-kit receptor in neuroblastomas and colorectal cancers using stem cell factor (SCF)-based recombinant bacterial toxins

Choudhary

Pardo

Rosinke

et al. 2015

Appl Microbiol Biotechnol

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Autocrine activation of c-kit (KIT receptor tyrosine kinase) has been postulated to be a potent oncogenic driver in small cell lung cancer, neuroblastoma (NB), and poorly differentiated colorectal carcinoma (CRC). Although targeted therapy involving tyrosine kinase inhibitors (TKIs) such as imatinib mesylate is highly effective for gastrointestinal stromal tumor carrying V560G c-kit mutation, it does not show much potential for targeting wild-type KIT (WT-KIT). Our study demonstrates the role of stem cell factor (SCF)-based toxin conjugates for targeting WT-KIT-overexpressing malignancies such as NBs and CRCs. We constructed SCF-based recombinant bacterial toxins by genetically fusing mutated form of natural ligand SCF to receptor binding deficient forms of Diphtheria toxin (DT) or Pseudomonas exotoxin A (ETA') and evaluated their efficacy in vitro. Efficient targeting was achieved in all receptor-positive neuroblastoma (IMR-32 and SHSY5Y) and colon cancer cell lines (COLO 320DM, HCT 116, and DLD-1) but not in receptor-negative breast carcinoma cell line (MCF-7) thereby proving specificity. While dose- and time-dependent cytotoxicity was observed in both neuroblastoma cell lines, COLO 320DM and HCT 116 cells, only an anti-proliferative effect was observed in DLD-1 cells. We prove that these novel targeting agents have promising potential as KIT receptor tyrosine kinase targeting system.

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“…CSC демонстрируют высокий уровень экспрессии белков, принадлежащих семейству мембранных ABC-транспортеров, вовлеченных в обеспечение резистент-ности к ХТ (в том числе паклитакселом, цисплатином, 5-фторурацилом, митоксантроном, антрациклинами, этопозидом, алкалоидом барвинка, камптотецином, то-потеканом и иматинибом) [19]. Уникальные свойства CSC могут объяснить неудачи множества методов противоопухолевой терапии, направленной на быст-роделящиеся клетки, так как CSC делятся медленно и нечувствительны к большинству цитотоксических препаратов [17].…”

Section: пути канцерогенеза толстой кишкиunclassified

Role of stem cells in large bowel carcinogenesis

Нефёдова¹,

Мальков²

2015

Onkol. koloproktol.

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Colon cancer stem cells – From basic to clinical application

Cited by 57 publications

References 205 publications

Elaidic Acid, a <b><i>Trans</i></b>-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells

Elaidic Acid, a <b><i>Trans</i></b>-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells

Targeting c-kit receptor in neuroblastomas and colorectal cancers using stem cell factor (SCF)-based recombinant bacterial toxins

Role of stem cells in large bowel carcinogenesis

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