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 Interleukin-6 promotes dietary carcinogen-induced DNA damage in colorectal cancer cells

2015 ◽  
Vol 4 (4) ◽  
pp. 858-866 ◽  
Author(s):  
Saroor A. A. Patel ◽  
Nigel J. Gooderham
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Interleukin 6 ◽  
Inflammatory Cytokine ◽  
Cultured Cells ◽  
Colorectal Cancer Cells ◽  
2D And 3D

Pro-inflammatory cytokine interleukin-6 promotes dietary carcinogen-mediated DNA damage in 2D and 3D cultured cells by inducingCYP1B1expression through miR27b downregulation.

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 Interleukin 6 Alters Localization of hMSH3, Leading to DNA Mismatch Repair Defects in Colorectal Cancer Cells

2015 ◽  
Vol 148 (3) ◽  
pp. 579-589 ◽  
Author(s):  
Stephanie S. Tseng-Rogenski ◽  
Yasushi Hamaya ◽  
Daniel Y. Choi ◽  
John M. Carethers
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Mismatch Repair ◽  
Interleukin 6 ◽  
Dna Mismatch Repair ◽  
Dna Mismatch ◽  
Colorectal Cancer Cells

Combination of TNF-α and graphene oxide-loaded BEZ235 to enhance apoptosis of PIK3CA mutant colorectal cancer cells

2013 ◽  
Vol 1 (41) ◽  
pp. 5602 ◽  
Author(s):  
Yuhua Cao ◽  
Yu Chong ◽  
He Shen ◽  
Mengxin Zhang ◽  
Jie Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Graphene Oxide ◽  
Cancer Cells ◽  
Tnf Α ◽  
Colorectal Cancer Cells

scholarly journals Kanglaite inhibits EMT caused by TNF-α via NF-κΒ inhibition in colorectal cancer cells

Oncotarget ◽  
2017 ◽  
Vol 9 (6) ◽  
pp. 6771-6779 ◽  
Author(s):  
Guiling Shi ◽  
Xiaoli Zheng ◽  
Shiwu Zhang ◽  
Xiaojing Wu ◽  
Fei Yu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Tnf Α ◽  
Colorectal Cancer Cells

scholarly journals The Role of Tumor Microenvironment Cells in Colorectal Cancer (CRC) Cachexia

2021 ◽  
Vol 22 (4) ◽  
pp. 1565
Author(s):  
Aldona Kasprzak
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Systemic Inflammation ◽  
Cancer Cachexia ◽  
Current Knowledge ◽  
Colorectal Cancer Cells ◽  
Factor Α ◽  
Cellular Components

Cancer cachexia (CC) is a multifactorial syndrome in patients with advanced cancer characterized by weight loss via skeletal-muscle and adipose-tissue atrophy, catabolic activity, and systemic inflammation. CC is correlated with functional impairment, reduced therapeutic responsiveness, and poor prognosis, and is a major cause of death in cancer patients. In colorectal cancer (CRC), cachexia affects around 50–61% of patients, but remains overlooked, understudied, and uncured. The mechanisms driving CC are not fully understood but are related, at least in part, to the local and systemic immune response to the tumor. Accumulating evidence demonstrates a significant role of tumor microenvironment (TME) cells (e.g., macrophages, neutrophils, and fibroblasts) in both cancer progression and tumor-induced cachexia, through the production of multiple procachectic factors. The most important role in CRC-associated cachexia is played by pro-inflammatory cytokines, including the tumor necrosis factor α (TNFα), originally known as cachectin, Interleukin (IL)-1, IL-6, and certain chemokines (e.g., IL-8). Heterogeneous CRC cells themselves also produce numerous cytokines (including chemokines), as well as novel factors called “cachexokines”. The tumor microenvironment (TME) contributes to systemic inflammation and increased oxidative stress and fibrosis. This review summarizes the current knowledge on the role of TME cellular components in CRC-associated cachexia, as well as discusses the potential role of selected mediators secreted by colorectal cancer cells in cooperation with tumor-associated immune and non-immune cells of tumor microenvironment in inducing or potentiating cancer cachexia. This knowledge serves to aid the understanding of the mechanisms of this process, as well as prevent its consequences.

scholarly journals IL-24-armed oncolytic vaccinia virus exerts potent antitumor effects via multiple pathways in colorectal cancer

2020 ◽  
Author(s):  
Lili Deng ◽  
Xue Yang ◽  
Jun Fan ◽  
Yuedi Ding ◽  
Ying Peng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Vaccinia Virus ◽  
Cancer Cells ◽  
Treatment Options ◽  
Antitumor Effects ◽  
Colorectal Cancer Cells ◽  
Cancer Tumor ◽  
Induced Apoptosis

Colorectal cancer is an aggressive malignancy for which there are limited treatment options. Oncolytic vaccinia virus isbeing developed as a novel strategy for cancer therapy. Arming vaccinia virus with immunostimulatory cytokines can enhance the tumor cell-specific replication and antitumor efficacy. Interleukin-24 (IL-24) is an important immune mediator, as well as a broad-spectrum tumor suppressor. Here, we constructed a targeted vaccinia virus of Guang9 strain harbored IL-24 (VG9-IL-24) to evaluate its antitumor effects. In vitro, VG9-IL-24 induced increased number of apoptotic cells and blocked colorectal cancer cells in the G2/M phase of the cell cycle. VG9-IL-24 induced apoptosis in colorectal cancer cells via multiple apoptotic signaling pathways. In vivo,VG9-IL-24 significantly inhibited the tumor growth and prolonged the survival both in human and murine colorectal cancer models. Besides, VG9-IL-24 stimulated multiple antitumor immune responses and direct bystander antitumor activity. Our results indicate that VG9-IL-24 can inhibit the growth of colorectal cancer tumor by inducing oncolysis and apoptosis as well as stimulating the anti-tumor immune effects. These findings indicate that VG9-IL-24 may exert a potential therapeutic strategy for combating colorectal cancer

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