scholarly journals Extracellular Metabolites Profile of Different Stages Colorectal Cancer Cell Lines

2021 ◽  
Vol 15 (2) ◽  
pp. 26-41
Author(s):  
Hazwani Mohd Yusof ◽  
◽  
Sharaniza Ab-Rahim ◽  
Wan Zurinah Wan Ngah ◽  
Sheila Nathan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metabolic Pathway Analysis ◽  
Molecular Changes ◽  
Extracellular Metabolites ◽  
Colorectal Cancer Cell Lines ◽  
Advanced Stages ◽  
The Media ◽  
Hct 116 ◽  
Metabolic Footprinting

Metabolic footprinting involves the determination of metabolites excreted or secreted by the cells. This study aimed to identify the differential extracellular metabolites in colorectal cancer (CRC) cells for the determination of molecular changes that occur as CRC progresses. CRC cells at different stages ie; SW 1116 (stage A), HT 29 and SW 480 (stage B), HCT 15 and DLD-1 (stage C), and HCT 116 (stage D) were grown in culture. The media in which the cells were grown are subjected to metabolomics profiling using Liquid Chromatography Mass Spectrometry-Quadrupole Time of Flight (LC/MS Q-TOF). Statistical and metabolic pathway analysis was performed using Metaboanalyst software and identification of metabolites was determined by the METLIN database. A total of 27 differential extracellular metabolites were identified in CRC cells of different stages compared to stage A cells. Data from the Partial least squares-discriminant analysis (PLS-DA) score plot shows a clear separation between CRC cells of different stages with a few overlaps between stage B and C. Further analysis using variable importance in projection (VIP) revealed 14 differential extracellular metabolites that were most significant in differentiating CRC cells of the advanced stages from stage A which are 5-hydroxy-L-tryptophan, indoleacetaldehyde, 4,5-dimethylthiazole, 8-oxodiacetoxyscirpenol, bisnorbiotin, 5-amino-6-(5'phosphoribosylamino) uracil, glyceryl 5-hydroxydecanoate, sphinganine, 8,8-diethoxy-2,6-dimethyl-2-octanol, l-cystine, thiamine acetic acid, phytosphingosine, PE (20:4(5Z,8Z,11Z,14Z)/22:6(4Z,7Z,10Z,13Z,16Z,19Z)), N-(2R-hydroxypentacosano-yl)-2S-amino-1,3S,4R-octadecanetriol. The different expressions of metabolites may indicate altered metabolic pathways in the more advanced CRC cells compared to stage A. This study highlights the importance of conducting both metabolomics profiling of extracellular and intracellular to generate a more complete understanding on the molecular changes that occur as CRC progresses.

scholarly journals Effects of radiofrequency radiation on colorectal cancer cell proliferation and inflammation

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Elcin Ozgur ◽  
Handan Kayhan ◽  
Gorkem Kismali ◽  
Fatih Senturk ◽  
Merve Sensoz ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
Colorectal Cancer Cell ◽  
Radiofrequency Radiation ◽  
Protein Levels ◽  
Intermittent Exposure ◽  
Colorectal Cancer Cells ◽  
Colorectal Cancer Cell Lines ◽  
Hct 116 ◽  
Hct 116 Cells

Abstract Objectives The aim of this study is to investigate the effects of radiofrequency radiation (RFR) on apoptosis, proliferation, stress response, and inflammation markers in colorectal cancer cells. Methods We tested the effects of intermittent exposure to RFR at different frequencies on two different colorectal cancer cell lines; HCT-116 and DLD-1. Protein levels were subsequently analyzed by ELISA. Results RFR led to a decrease in P53, p-P53, p-P38, and p-IkB levels in HCT-116 cells, while leading to an increase in BAD, p-BAD, p-STAT3,NF-κB levels. Two thousand one hundred Megahertz of RFR altered the P53, BAD, and NF-ΚB expression in HCT-116 cells. P53, p-P53, BAD, p-BAD, NF-κB, p-NF-κB, p-P38, p-SAPK/JNK, p-STAT3, and p-IkB levels increased after exposure to RFR at 900 and 2,100 MHz in DLD-1 cells. Unlike HCT-116 cells, 1,800 MHz of RFR was reported to have no effect on DLD1 cells. Conclusions RFR increased apoptosis and inflammatory response in HCT116 cells, while lowering the active P38 and active P53 levels, which are indicators of poor prognosis in several cancers. Genetic differences, such as P53 mutation (DLD-1), are critical to the cell response to RFR, which explains the reason why scientific studies on the effects of RFR yield contradictory results.

scholarly journals THE HDAC INHIBITOR SODIUM PHENYLBUTYRATE ENHANCES THE CYTOTOXICITY INDUCED BY 5-FLUOROURACIL, OXALIPLATIN, AND IRINOTECAN IN COLORECTAL CANCER CELL LINES

2018 ◽  
Vol 10 (1) ◽  
pp. 155
Author(s):  
Maha S. Al-keilani ◽  
Dua H. Alsmadi
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
P Value ◽  
Mutant P53 ◽  
Colorectal Cancer Cell Lines ◽  
Hct 116 ◽  
Ht 29

Objective: The main objective of this study was to evaluate the ability of sodium phenylbutyrate (NaPB) to enhance the cytotoxicity of 5-fluorouracil, oxaliplatin, and irinotecan against colorectal cancer cell lines expressing wild-type and mutant p53.Methods: The antiproliferative effect of NaPB alone or in combination with 5-fluorouracil, oxaliplatin, or irinotecan in HCT-116 and HT-29 colorectal cancer cell lines was investigated using the MTT cell proliferation assay. IC50 values were calculated using Compusyn Software 1.0 (Combosyn Inc.). Synergy values (R) were calculated using the ratio of IC50 of each primary drug alone divided by combination IC50s. For each two pairs of experiments, student’s t-test was used for analysis. In combination studies, one-way ANOVA test; Tukey post-hoc testing was performed using R 3.3.2 software. P-value<0.05 was considered significant.Results: NaPB inhibited the growth of HCT-116 and HT-29 cell lines in a dose-dependent manner (IC50s 4.7 mmol, and 10.1 mmol, respectively). HT-29 cell lines (mutant p53) were more sensitive to NaPB at low concentrations (<4 mmol). Moreover, the addition of NaPB to HCT-116 and HT-29 with 5-fluorouracil, oxaliplatin, or irinotecan synergistically induced the antiproliferative effect (R>1.6, p-value<0.05).Conclusion: NaPB enhanced the cytotoxicity of conventional chemotherapy against colorectal cancer cell lines harboring wild-type or mutant p53. Thus NaPB is a promising potential adjuvant chemotherapy in colorectal cancer.

scholarly journals N-Glycoproteins Have a Major Role in MGL Binding to Colorectal Cancer Cell Lines: Associations with Overall Proteome Diversity

2020 ◽  
Vol 21 (15) ◽  
pp. 5522 ◽  
Author(s):  
Martina Pirro ◽  
Yassene Mohammed ◽  
Sandra J. van Vliet ◽  
Yoann Rombouts ◽  
Agnese Sciacca ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Quantitative Proteomics ◽  
Transcriptional Factor ◽  
Protein Glycosylation ◽  
Promising Tool ◽  
Colorectal Cancer Cell Lines ◽  
Advanced Stages ◽  
Type C ◽  
The Impact

Colorectal cancer (CRC) is the second-leading cause of cancer death worldwide due in part to a high proportion of patients diagnosed at advanced stages of the disease. For this reason, many efforts have been made towards new approaches for early detection and prognosis. Cancer-associated aberrant glycosylation, especially the Tn and STn antigens, can be detected using the macrophage galactose-type C-type lectin (MGL/CLEC10A/CD301), which has been shown to be a promising tool for CRC prognosis. We had recently identified the major MGL-binding glycoproteins in two high-MGL-binding CRC cells lines, HCT116 and HT29. However, we failed to detect the presence of O-linked Tn and STn glycans on most CRC glycoproteins recognized by MGL. We therefore investigated here the impact of N-linked and O-linked glycans carried by these proteins for the binding to MGL. In addition, we performed quantitative proteomics to study the major differences in proteins involved in glycosylation in these cells. Our results showed that N-glycans have a significant, previously underestimated, importance in MGL binding to CRC cell lines. Finally, we highlighted both common and cell-specific processes associated with a high-MGL-binding phenotype, such as differential levels of enzymes involved in protein glycosylation, and a transcriptional factor (CDX-2) involved in their regulation.

scholarly journals METABOLITES PROFILE OF COLORECTAL CANCER CELLS AT DIFFERENT STAGES

2019 ◽  
pp. 66-70
Author(s):  
HAZWANI MOHD YUSOF ◽  
SHARANIZA AB-RAHIM ◽  
WAN ZURINAH WAN NGAH ◽  
SHEILA NATHAN ◽  
RAHMAN A JAMAL A ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Therapeutic Interventions ◽  
Flavin Mononucleotide ◽  
Therapeutic Drug ◽  
Liquid Chromatography Mass Spectrometry ◽  
Colorectal Cancer Cells ◽  
Metabolite Profiles ◽  
Advanced Stages ◽  
Hct 116 ◽  
Ht 29

Objective: The aim of this study is to characterize the metabolite profiles of colorectal cancer (CRC) cells of different stages of the disease to understandthe pathophysiological changes that may help to identify prevention strategies as well as the sites for potential therapeutic drug actions.Methods: Six CRC cell lines of different stages (classified using the Dukes classification) were used, and they are SW 1116 (stage A), HT 29 and SW480 (stage B), HCT 15 and DLD-1 (stage C), and HCT 116 (stage D). Metabolites were extracted using methanol and water, and metabolic profiling wasperformed using liquid chromatography-mass spectrometry. Mass profiler professional software was used for statistical analysis.Results: There were 111,096 compounds detected across the samples, and 24 metabolites were identified to be significantly different betweenthe CRC stages. Most notably, there were eight metabolites that were significantly upregulated in the more advanced stages (B, C, and D) comparedwith Stage A. These metabolites include flavin mononucleotide, l-methionine, muricatacin, amillaripin, 2-methylbutyroylcarnitine, lumichrome,hexadeconoic acid, and lysoPE (0:0/16:0).Conclusion: This study showed that the expressions of metabolites at different stages of CRC were different, which represent the metabolic changesoccurring as CRC advances. The knowledge may help identify biomarkers for the staging of CRC, which could improve its prognosis as well as providea basis for the development of therapeutic interventions.

scholarly journals L-Glutaminase Synthesis by Marine Halomonas meridiana Isolated from the Red Sea and Its Efficiency against Colorectal Cancer Cell Lines

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1963
Author(s):  
Yasser S. Mostafa ◽  
Saad A. Alamri ◽  
Mohammad Y. Alfaifi ◽  
Sulaiman A. Alrumman ◽  
Serag Eldin I. Elbehairi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Red Sea ◽  
Specific Activity ◽  
Kinetics Parameters ◽  
Toxic Activity ◽  
Highly Active ◽  
Colorectal Cancer Cell Lines ◽  
Late Apoptosis ◽  
Hct 116 ◽  
Cancer Agent

L-glutaminase is an important anticancer agent that is used extensively worldwide by depriving cancer cells of L-glutamine. The marine bacterium, Halomonas meridian was isolated from the Red Sea and selected as the more active L-glutaminase-producing bacteria. L-glutaminase fermentation was optimized at 36 h, pH 8.0, 37 °C, and 3.0% NaCl, using glucose at 1.5% and soybean meal at 2%. The purified enzyme showed a specific activity of 36.08 U/mg, and the molecular weight was found to be 57 kDa by the SDS-PAGE analysis. The enzyme was highly active at pH 8.0 and 37 °C. The kinetics’ parameters of Km and Vmax were 12.2 × 10−6 M and 121.95 μmol/mL/min, respectively, which reflects a higher affinity for its substrate. The anticancer efficiency of the enzyme showed significant toxic activity toward colorectal adenocarcinoma cells; LS 174 T (IC50 7.0 μg/mL) and HCT 116 (IC50 13.2 μg/mL). A higher incidence of cell death was observed with early apoptosis in HCT 116 than in LS 174 T, whereas late apoptosis was observed in LS 174 T more than in HCT 116. Also, the L-glutaminase induction nuclear fragmentation in HCT 116 was more than that in the LS 174T cells. This is the first report on Halomonas meridiana as an L-glutaminase producer that is used as an anti-colorectal cancer agent.

A panel of mono- and dinucleotide microsatellite markers is required for reliable determination of the MSI status in colorectal cancer

2001 ◽  
Vol 120 (5) ◽  
pp. A599-A599
Author(s):  
C ARNOLD ◽  
A GOEL ◽  
J CARETHERS ◽  
L WASSERMAN ◽  
C COMPTON ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Microsatellite Markers ◽  
Reliable Determination

Bioactive Peptides Sensitize Cells to Anticancer Effects of Oxaliplatin in Human Colorectal Cancer Xenografts in Nude Mice

2019 ◽  
Vol 26 (7) ◽  
pp. 512-522
Author(s):  
Xian Li ◽  
Long Xia ◽  
Xiaohui Ouyang ◽  
Qimuge Suyila ◽  
Liya Su ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Colorectal Cancer ◽  
Nude Mice ◽  
Low Dose ◽  
Bioactive Peptides ◽  
Human Colorectal Cancer ◽  
Short Term ◽  
Hct 116

<P>Background: Despite new agent development and short-term benefits in patients with Colorectal Cancer (CRC), metastatic CRC cure rates have not improved due to high rates of oxaliplatin resistance and toxicity. There is an urgent need for effective tools to prevent and treat CRC and reduce morbidity and mortality of CRC patients. Exploring the effects of bioactive peptides on the antitumor to CRC was of vital importance to the clinical application. </P><P> Objective: This study aimed to investigate the therapeutic impact of Anticancer Bioactive Peptides (ACBP) on anticancer effect of oxaliplatin (LOHP) in human colorectal cancer xenografts models in nude mice. </P><P> Methods: HCT-116 cells were cultured in vitro via CCK-8 assays and the absorbance was measured at 450 nm. Apoptosis and cell cycle were assessed by Flow Cytometry (FCM) in vitro. HCT-116 human colorectal cancer cells inoculated subcutaneously in nude mice of treatment with PBS (GG), ACBP, LOHP, ACBP+LOHP (A+L) in vivo. The quality of life was assessed by dietary amount of nude mice, the weight of nude mice, inhibition rates, tumor weight and tumor volume. Immunohistochemistry and RT-qPCR method was conducted to determine the levels of apoptosisregulating proteins/genes in transplanted tumors. </P><P> Results: ACBP induced substantial reductions in viable cell numbers and apoptosis of HCT116 cells in combined with LOHP in vitro. Compared with the control GG group, ACBP combined low dose oxaliplatin (U) group demonstrated significantly different tumor volume, the rate of apoptosis, the expression levels of Cyt-C, caspase-3,8,9 proteins and corresponding RNAs (P<0.05). The expression of pro-apoptotic proteins in the cytoplasm around the nucleus was significantly enhanced by ACBP. Short term intermittent use of ACBP alone indicted a certain inhibitory effect on tumor growth, and improve the quality of life of tumor bearing nude mice. </P><P> Conclusion: ACBP significantly increased the anti-cancer responses of low dose oxaliplatin (L-LOHP), thus, significantly improving the quality of life of tumor-bearing nude mice.</P>

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