scholarly journals Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts

10.3791/51475 ◽  
2014 ◽  
Author(s):  
Marc D. Bullock ◽  
Max Mellone ◽  
Karen M. Pickard ◽  
Abdulkadir Emre Sayan ◽  
Richard Mitter ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Ex Vivo ◽  
Molecular Profiling ◽  
Dimensional Model ◽  
Invasive Tumor ◽  
3 Dimensional ◽  
Colorectal Cancer Cells

Cold atmospheric plasma treatment inhibits growth in colorectal cancer cells

2018 ◽  
Vol 400 (1) ◽  
pp. 111-122 ◽  
Author(s):  
Christin Schneider ◽  
Stephanie Arndt ◽  
Julia L. Zimmermann ◽  
Yangfang Li ◽  
Sigrid Karrer ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Plasma Treatment ◽  
Cancer Cells ◽  
Ex Vivo ◽  
Atmospheric Plasma ◽  
Normal Colon ◽  
Colon Tissue ◽  
Cold Atmospheric Plasma ◽  
Colorectal Cancer Cells

AbstractPlasma oncology is a relatively new field of research. Recent developments have indicated that cold atmospheric plasma (CAP) technology is an interesting new therapeutic approach to cancer treatment. In this study, p53 wildtype (LoVo) and human p53 mutated (HT29 and SW480) colorectal cancer cells were treated with the miniFlatPlaSter – a device particularly developed for the treatment of tumor cells – that uses the Surface Micro Discharge (SMD) technology for plasma production in air. The present study analyzed the effects of plasma on colorectal cancer cellsin vitroand on normal colon tissueex vivo. Plasma treatment had strong effects on colon cancer cells, such as inhibition of cell proliferation, induction of cell death and modulation of p21 expression. In contrast, CAP treatment of murine colon tissueex vivofor up to 2 min did not show any toxic effect on normal colon cells compared to H2O2positive control. In summary, these results suggest that the miniFlatPlaSter plasma device is able to kill colorectal cancer cells independent of their p53 mutation status. Thus, this device presents a promising new approach in colon cancer therapy.

scholarly journals ANKRD22, a novel tumor microenvironment-induced mitochondrial protein promotes metabolic reprogramming of colorectal cancer cells

Theranostics ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 516-536
Author(s):  
Tianhui Pan ◽  
Jingwen Liu ◽  
Song Xu ◽  
Qiao Yu ◽  
Hongping Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Mitochondrial Protein ◽  
Metabolic Reprogramming ◽  
Colorectal Cancer Cells

scholarly journals IL6 Modulates the Immune Status of the Tumor Microenvironment to Facilitate Metastatic Colonization of Colorectal Cancer Cells

2019 ◽  
Vol 7 (12) ◽  
pp. 1944-1957 ◽  
Author(s):  
Yujiro Toyoshima ◽  
Hidemitsu Kitamura ◽  
Huihui Xiang ◽  
Yosuke Ohno ◽  
Shigenori Homma ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Immune Status ◽  
Metastatic Colonization ◽  
Colorectal Cancer Cells

scholarly journals TNF-alpha Induces Pro-Inflammatory Factors in Colorectal Cancer Microenvironment

2020 ◽  
Vol 7 (4) ◽  
pp. 466-469
Author(s):  
Ahu Pakdemirli ◽  
Gizem Calibasi Kocal
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Interleukin 6 ◽  
Interleukin 8 ◽  
Soluble Factors ◽  
Tnf Α ◽  
Colorectal Cancer Cells ◽  
Cancer Tumor ◽  
Cellular Components

Objective: The tumor microenvironment has a crucial role in organizing cancer malignancy, progression, drug resistance and survival. It consists of cellular and non-cellular components. These non-cellular components such as cytokines, extracellular matrix, growth factors and metabolites are responsible for shifting the action from pro-cancer to anti-cancer effects. Twenty percent of all cancers occur in association with chronic inflammation via cytokines. Even cancers that are not caused by chronic inflammation, present high levels of cytokine expression pattern in their tumor microenvironment. Tumor necrosis factor-alpha (TNF-α) and some interleukins are characterized as pro-tumorigenic cytokines and they were involved in cancer by presenting their ability to activate the oncogenic transcription factors. The aim of this study is to evaluate the remodeling of colorectal cancer tumor microenvironment by TNF-α. Material and Methods: TNF-α (5ng/ml) was applied to HT-29 colorectal cancer cells, then human soluble factors were determined by using Human Cytokine Group 1, 8 plex Panel (Bio-Rad Laboratories Inc. USA) and Magpix Luminex instrument and xPONENT software (version 4.2, Luminex Corp, Austin, Texas, US). The results were normalized to total protein concentration estimated via Bradford assay. Results: Current research highlights the effect of TNF-α on the tumor microenvironment.  Interleukin-6 and interleukin -8 soluble factors were higher in TNF-α treated colorectal cancer cells when compared with untreated control group. Conclusion: The results of the study show that TNF-α is responsible for elevating the levels of interleukin-6 and interleukin-8, which are associated with inflammation in the tumor microenvironment. Key words: Colorectal Cancer, Tumor Microenvironment, Cytokines, TNF-α, Interleukin-6, interleukin -8

scholarly journals Resveratrol Suppresses Cross-Talk between Colorectal Cancer Cells and Stromal Cells in Multicellular Tumor Microenvironment: A Bridge between In Vitro and In Vivo Tumor Microenvironment Study

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4292
Author(s):  
Constanze Buhrmann ◽  
Parviz Shayan ◽  
Aranka Brockmueller ◽  
Mehdi Shakibaei
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
T Lymphocytes ◽  
Cancer Cells ◽  
T Lymphocyte ◽  
Stromal Cells ◽  
Colorectal Cancer Cells ◽  
Hct116 Cells

The interaction between tumor cells and the tumor microenvironment (TME) is an important process for the development of tumor malignancy. Modulation of paracrine cross-talk could be a promising strategy for tumor control within the TME. The exact mechanisms of multi-targeted compound resveratrol are not yet fully understood. Whether resveratrol can modulate paracrine signal transduction-induced malignancy in the multicellular-TME of colorectal cancer cells (CRC) was investigated. An in vitro model with 3D-alginate HCT116 cells in multicellular-TME cultures (fibroblast cells, T-lymphocytes) was used to elucidate the role of TNF-β, Sirt1-ASO and/or resveratrol in the proliferation, invasion and cancer stem cells (CSC) of CRC cells. We found that multicellular-TME, similar to TNF-β-TME, promoted proliferation, colony formation, invasion of CRC cells and enabled activation of CSCs. However, after co-treatment with resveratrol, the malignancy of multicellular-TME reversed to HCT116. In addition, resveratrol reduced the secretion of T-lymphocyte/fibroblast (TNF-β, TGF-β3) proteins, antagonized the T-lymphocyte/fibroblast-promoting NF-κB activation, NF-κB nuclear translocation and thus the expression of NF-κB-promoting biomarkers, associated with proliferation, invasion and survival of CSCs in 3D-alginate cultures of HCT116 cells induced by TNF-β- or multicellular-TME, but not by Sirt1-ASO, indicating the central role of this enzyme in the anti-tumor function of resveratrol. Our results suggest that in vitro multicellular-TME promotes crosstalk between CRC and stromal cells to increase survival, migration of HCT116 and the resveratrol/Sirt1 axis suppresses this loop by modulating paracrine agent secretion and NF-κB signaling. Fibroblasts and T-lymphocytes are promising targets for resveratrol in the prevention of CRC metastasis.

Hypoxic colorectal cancer-secreted exosomes deliver miR-210-3p to normoxic tumor cells to elicit a protumoral effect

2021 ◽  
pp. 153537022110115
Author(s):  
Liuqing Ge ◽  
Feng Zhou ◽  
Jiayan Nie ◽  
Xiaobing Wang ◽  
Qiu Zhao
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Preclinical Study ◽  
Mechanistic Investigation ◽  
Colorectal Cancer Cells ◽  
Colorectal Cancer Progression

Hypoxia, the most common feature in the tumor microenvironment, is closely related to tumor malignant progression and poor patient’s prognosis. Exosomes, initially recognized as cellular “garbage dumpsters”, are now known to be important mediums for mediating cellular communication in tumor microenvironment. However, the mechanisms of hypoxic tumor cell-derived exosomes facilitate colorectal cancer progression still need further exploration. In the present study, we found that exosomes from hypoxic colorectal cancer cells (H-Exos) promoted G1-S cycle transition and proliferation while preventing the apoptosis of colorectal cancer cells by transmitting miR-210-3p to normoxic tumor cells. Mechanistic investigation indicated that miR-210-3p from H-Exos elicited its protumoral effect via suppressing CELF2 expression. A preclinical study further confirmed that H-Exos could promote tumorigenesis in vivo. Clinically, the expression of miR-210-3p in circulating plasma exosomes was markedly upregulated in colorectal cancer patients, which were closely associated with multiple unfavorable clinicopathological features. Taken together, these results suggest that hypoxia may stimulate colorectal cancer cells to secrete miR-210-3p-enriched exosomes in tumor microenvironment, which elicit protumoral effects by inhibiting CELF2 expression. These findings provide new insights on the mechanism of colorectal cancer progression and potential therapeutic targets for colorectal cancer.

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