Effects of radiofrequency radiation on colorectal cancer cell proliferation and inflammation

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.

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An Integrated Bioinformatics Analysis Repurposes an Antihelminthic Drug Niclosamide for Treating HMGA2-Overexpressing Human Colorectal Cancer

Cancers ◽

10.3390/cancers11101482 ◽

2019 ◽

Vol 11 (10) ◽

pp. 1482 ◽

Cited By ~ 6

Author(s):

Leung ◽

Chou ◽

Huang ◽

Yang

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Cell Lines ◽

Cancer Cell ◽

Gene Signature ◽

Cancer Cell Lines ◽

Colorectal Cancer Cell ◽

Sequencing Analysis ◽

Colorectal Cancer Cells ◽

Colorectal Cancer Cell Lines

Aberrant overexpression of high mobility group AT-hook 2 (HMGA2) is frequently found in cancers and HMGA2 has been considered an anticancer therapeutic target. In this study, a pan-cancer genomics survey based on Cancer Cell Line Encyclopedia (CCLE) and The Cancer Genome Atlas (TCGA) data indicated that HMGA2 was mainly overexpressed in gastrointestinal cancers including colorectal cancer. Intriguingly, HMGA2 overexpression had no prognostic impacts on cancer patients’ overall and disease-free survivals. In addition, HMGA2-overexpressing colorectal cancer cell lines did not display higher susceptibility to a previously identified HMGA2 inhibitor (netroposin). By microarray profiling of HMGA2-driven gene signature and subsequent Connectivity Map (CMap) database mining, we identified that S100 calcium-binding protein A4 (S100A4) may be a druggable vulnerability for HMGA2-overexpressing colorectal cancer. A repurposing S100A4 inhibitor, niclosamide, was found to reverse the HMGA2-driven gene signature both in colorectal cancer cell lines and patients’ tissues. In vitro and in vivo experiments validated that HMGA2-overexpressing colorectal cancer cells were more sensitive to niclosamide. However, inhibition of S100A4 by siRNAs and other inhibitors was not sufficient to exert effects like niclosamide. Further RNA sequencing analysis identified that niclosamide inhibited more cell-cycle-related gene expression in HMGA2-overexpressing colorectal cancer cells, which may explain its selective anticancer effect. Together, our study repurposes an anthelminthic drug niclosamide for treating HMGA2-overexpression colorectal cancer.

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Surface-bound galectin-4 regulates gene transcription and secretion of chemokines in human colorectal cancer cell lines

Tumor Biology ◽

10.1177/1010428317691687 ◽

2017 ◽

Vol 39 (3) ◽

pp. 101042831769168 ◽

Cited By ~ 5

Author(s):

U Subrahmanyeswara Rao ◽

Prema S Rao

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Cell Surface ◽

Cancer Cells ◽

Cell Lines ◽

Cancer Cell ◽

Colorectal Cancer Cell ◽

Colorectal Tumorigenesis ◽

Colorectal Cancer Cells ◽

Colorectal Cancer Cell Lines

One long-term complication of chronic intestinal inflammation is the development of colorectal cancer. However, the mechanisms linking inflammation to the colorectal tumorigenesis are poorly defined. Previously, we have demonstrated that galectin-4 is predominantly expressed in the luminal epithelia of the gastrointestinal tract, and its loss of expression plays a key role in the colorectal tumorigenesis. However, the mechanism by which galectin-4 regulates inflammation-induced tumorigenesis is unclear. Here, we show that galectin-4 secreted by the colorectal cancer cell lines was bound to the cell surface. Neutralization of surface-bound galectin-4 with anti-galectin-4 antibody resulted in increased cell proliferation with concomitant secretion of several chemokines into the extracellular medium. Neutralization of the surface-bound galectin-4 also resulted in the up-regulation of transcription of 29 genes, several of which are components of multiple inflammation signaling pathways. In an alternate experiment, binding of recombinant galectin-4 protein to cell surface of the galectin-4-negative colorectal cancer cells resulted in increased p27, and decreased cyclin D1 and c-Myc levels, leading to cell cycle arrest and apoptosis. Together, these data demonstrated that surface-bound galectin-4 is a dual function protein—down-regulating cell proliferation and chemokine secretion in galectin-4-expressing colorectal cancer cells on one hand and inducing apoptosis in galectin-4-negative colorectal cancer cells on the other hand.

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Omentin-1 Promotes the Proliferation, Invasion, Migration and Angiogenesis of Colorectal Cancer Cells

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2019.2029 ◽

2019 ◽

Vol 9 (5) ◽

pp. 673-678

Author(s):

Hua Ye ◽

Hui Luo ◽

Yun Tu ◽

Liao Cui

Keyword(s):

Colorectal Cancer ◽

Western Blot ◽

Cancer Cells ◽

Cell Lines ◽

Cancer Cell ◽

Blot Analysis ◽

Western Blot Analysis ◽

Colorectal Cancer Cell ◽

Colorectal Cancer Cells ◽

Colorectal Cancer Cell Lines

Colorectal cancer (CRC) is one of the common malignant tumors of digestive system, which the incidence of CRC has been on the rise in recent years. Omentin-1 is reported to be increased in plasma of CRC patients. The present study aimed to investigate whether Omentin-1 could promote the proliferation, invasion, migration and angiogenesis of colorectal cancer cells. ELISA assay and western blot analysis detected the Omentin-1 level in plasma of CRC patients and western blot analysis and RT-qPCR analysis detected the Omentin-1 level in colorectal cancer cell lines. The transfection effects were verified by western blot analysis. The cell proliferation, invasion and migration were determined by CCK-8 assay, wound healing assay and transwell assay. The expression of MMP2, MMP9, VEGF and AngII was analyzed by western blot analysis. The results showed that Omentin-1 was increased in plasma of CRC patients and colorectal cancer cell lines. Omentin-1 overexpression promoted the proliferation, invasion, migration and angiogenesis of colorectal cancer cells. And, up-regulation of Omentin-1 increased the expression of MMP2, MMP9, VEGF and AngII. In conclusion, our data suggested that Omentin-1 promoted the proliferation, invasion, migration and angiogenesis of colorectal cancer cells.

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

International Journal of Pharmacy and Pharmaceutical Sciences ◽

10.22159/ijpps.2018v10i1.22947 ◽

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.

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