miR‐497‐5p mediates starvation‐induced death in colon cancer cells by targeting acyl‐CoA synthetase‐5 and modulation of lipid metabolism

2020 ◽  
Vol 235 (7-8) ◽  
pp. 5570-5589 ◽  
Author(s):  
Ehsan Gharib ◽  
Parinaz Nasri Nasrabadi ◽  
Mohammad Reza Zali
Keyword(s):  
Colon Cancer ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Colon Cancer Cells

Influence of butyrate on lipid metabolism, survival, and differentiation of colon cancer cells

1991 ◽  
Vol 16 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Atif B. Awad ◽  
Peter J. Horvath ◽  
Martha S. Andersen
Keyword(s):  
Colon Cancer ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Colon Cancer Cells

scholarly journals Integrated multi-omics approach reveals a role of ALDH1A1 in lipid metabolism in human colon cancer cells

2019 ◽  
Vol 304 ◽  
pp. 88-96 ◽  
Author(s):  
Georgia Charkoftaki ◽  
David C. Thompson ◽  
Jaya Prakash Golla ◽  
Rolando Garcia-Milian ◽  
TuKiet T. Lam ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

scholarly journals FABP4 promotes invasion and metastasis of colon cancer by regulating fatty acid transport

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Wenying Tian ◽  
Wenjia Zhang ◽  
Yan Zhang ◽  
Tianyue Zhu ◽  
Yuting Hua ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Akt Pathway ◽  
Colon Cancer Cells ◽  
Cancer Tissues ◽  
Adipose Tissue Extract

Abstract Background The prognosis of colon cancer is poor for metastasis, while the mechanism, especially adipocytes related, is not yet clear. The purpose of this study is to determine the effects of fatty acid binding protein 4 (FABP4), a transporter for lipids, on colon cancer progression. Methods The distribution of lipids and FABP4 was tested in the colon cancer tissues and adjacent normal tissues, and their relationship was also verified in vitro. Experiments about cellular invasion, migration and proliferation were performed to detect the impacts of FABP4 on the biological behaviors of colon cancer, and the positive results were checked in vivo. Meanwhile, the regulatory role of FABP4 in the energy and lipid metabolism was evaluated by the levels of triglyceride, ATP, LDH, glycerol and NEFA. At last, GO and KEGG analysis based on FABP4 overexpressed cells was performed, and the AKT pathway and epithelial–mesenchymal transition (EMT)-related proteins were determined by Western blot. Results Higher accumulation of lipids and stronger FABP4 transcription were observed in colon cancer tissues. Having been incubated with adipose tissue extract and overexpressed FABP4, colon cancer cells demonstrated enhanced lipid accumulation. In functional experiments, co-culture with adipose tissue extract significantly enhanced the invasion and migration of colon cancer cells, as well as the energy and lipid metabolism, and all these processes were reversed by FABP4 inhibitor. In addition, the metastasis of FABP4-overexpressed colon cancer cells was also significantly enhanced in vitro and in vivo. In terms of mechanism, the bioinformatics analysis showed that FABP4 was enriched in 11 pathways related to metabolic processes in FABP4 overexpressed cells. Finally, FABP4 overexpression improved EMT progression of colon cancer, as evidenced by the upregulation of Snail, MMP-2 and MMP-9, the downregulation of E-cadherin. The expression of p-Akt was also elevated. Conclusion FABP4 overexpression could increase FAs transport to enhance energy and lipid metabolism, and activate AKT pathway and EMT to promote the migration and invasion of colon cancer cells.

Leptin is a growth factor for human colon cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A493-A493
Author(s):  
J HARDWICK ◽  
G VANDENBRINK ◽  
S VANDEVENTER ◽  
M PEPPELENBOSCH
Keyword(s):  
Colon Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

Silencing of a death associated protein kinase as a pro-survival factor in colon cancer cells

Endoscopy ◽  
2005 ◽  
Vol 37 (05) ◽  
Author(s):  
GA Doherty ◽  
SM Byrne ◽  
SC Austin ◽  
GM Scully ◽  
EW Kay ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Survival Factor ◽  
Death Associated Protein Kinase

Cytotoxic Effect of the Combination of Gemcitabine and Atorvastatin Loaded in Microemulsion on the HCT116 Colon Cancer Cells

2017 ◽  
Vol 9 (2) ◽  
Author(s):  
Mayson H. Alkhatib ◽  
Dalal Al-Saedi ◽  
Wadiah S. Backer
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Therapeutic Potential ◽  
Morphological Changes ◽  
In Vitro Study ◽  
Colon Cancer Cells ◽  
Apoptosis Detection ◽  
Hct116 Cells

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.

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