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.

Serum Starvation Sensitizes Anticancer Effect of Anemarrhena asphodeloides via p38/JNK-Induced Cell Cycle Arrest and Apoptosis in Colorectal Cancer Cells

2021 ◽  
pp. 1-16
Author(s):  
Kon-Young Ji ◽  
Ki Mo Kim ◽  
Yun Hee Kim ◽  
Ki-Shuk Shim ◽  
Joo Young Lee ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Serum Starvation ◽  
Anticancer Effect ◽  
Cycle Arrest ◽  
Colorectal Cancer Cells ◽  
Anemarrhena Asphodeloides ◽  
Hct116 Cells

The molecular mechanism underlying the anticancer effects of Anemarrhena asphodeloides (A. asphodeloides) on colon cancer is unknown. This is the first study evaluating the anticancer effect of A. asphodeloides extract (AA-Ex) in serum-starved colorectal cancer cells. Changes in cell proliferation and morphology in serum-starved MC38 and HCT116 colorectal cancer cells were investigated using MTS assay. Cell cycle and apoptosis were investigated using flow cytometry, and cell cycle regulator expression was determined using qRT-PCR. Apoptosis regulator protein levels and mitogen-activated protein kinase (MAPK) phosphorylation were assessed using western blotting. AA-Ex sensitively suppressed proliferation of serum-starved colorectal cancer cells, with MC38 and HCT116 cells showing greater changes in proliferation after treatment with AA-Ex under serum starvation than HaCaT and RAW 264.7 cells. AA-Ex inhibited cell cycle progression in serum-starved MC38 and HCT116 cells and increased the expression of cell cycle inhibitors (p53, p21, and p27). Furthermore, AA-Ex induced apoptosis in serum-starved MC38 and HCT116 cells. Consistently, AA-Ex suppressed the expression of the anti-apoptotic molecule Bcl-2 and upregulated pro-apoptotic molecules (cytochrome c, cleaved caspase-9, cleaved caspase-3, and cleaved-PARP) in serum-starved cells. AA-Ex treatment under serum starvation decreased AKT and ERK1/2 phosphorylation in the cell survival signaling pathway but increased p38 and JNK phosphorylation. Furthermore, AA-Ex treatment with serum starvation increased the levels of the transcription factors of the p38 and JNK pathway. Serum starvation sensitizes colorectal cancer cells to the anticancer effect of A. asphodeloidesvia p38/JNK-induced cell cycle arrest and apoptosis. Hence, AA-Ex possesses therapeutic potential for colon cancer treatment.

scholarly journals Cortisol and Testosterone Induce Bax and Bcl-2 Gene Expression and Caspases-8 and -9 Activity in Colon Cancer Cells (ht29) and Reduced the Cell Viability

2021 ◽  
Author(s):  
Amin Sarkhosh ◽  
Rahim Ahmadi ◽  
Seyyed Hossein Khatami ◽  
Hadi Ghasemi
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Colorimetric Method ◽  
Caspase 8 ◽  
Activity Levels ◽  
Colon Cancer Cells ◽  
Expression Levels ◽  
Colorectal Cancer Cells ◽  
The Impact

Abstract Cortisol and testosterone can inhibit the proliferation of colorectal cancer cells. Cortisol may augment the anti-cancer activity of testosterone in colorectal cancer cells. This research aimed to assess the impact of cortisol and testosterone on the viability of colon cancer cells (HTCs). The cytotoxic effects of cortisol and testosterone were evaluated using the MTT assay. Bax and Bcl-2 expression levels were determined using real-time PCR. The colorimetric method was used to assess the activity of caspase-8 and -9 enzymes. The expression levels of Bax and Bcl-2 genes significantly increased (p<0.001), as well as the activity levels of caspase-8 and -9, were elevated (p<0.001). Testosterone may exert cytotoxic activity in colon cancer cells in the presence of cortisol, and cortisol and testosterone cotreatment may contribute to the elevated Bax and Bcl-2 genes expression and caspase 8 and 9 activity enhancement in colorectal cancer cells.

The Role of Interleukin-22 Receptor1 in the Proliferation and Apoptosis of Colonrectal Cancer

2021 ◽  
Vol 11 (1) ◽  
pp. 22-27
Author(s):  
Xiaoning Qin ◽  
Hongxun Ruan ◽  
Yinghao Hao ◽  
Weiqi Kong ◽  
Jing Zhao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Interleukin 22 ◽  
Nuclear Antigens ◽  
Proliferation And Apoptosis ◽  
Colorectal Cancer Cells ◽  
Before And After ◽  
And Control

Background: To study the relationship between interleukin-22 receptor1 (IL-22R1) and the proliferation and apoptosis of colon cancer cells. Methods: SW480, SW620 (Human Colorectal Cancer Cell Lines) that express positive to IL-22R1 were exposed in the environment of IL-22. The proliferation trial included 5 groups: IL-22, 5-FU, 5-FU + IL-22, medium and control. The apoptosis trial included 4 groups: IL-22, 5-FU, 5-FU + IL-22 and control. The result of apoptosis was detected by Apoptosis Kit (AnnxinVPE and 7-AAD), and proliferation was detected by Ki67 antibody (Cell proliferation-associated nuclear antigens). The rates of proliferation and apoptosis were detected by flow cytometry. Changes of the rate of proliferation and apoptosis before and after silencing were compared and analyzed statistically after silencing the gene of IL-22R1. Result: The combination of IL-22R1 and IL-22 could significantly inhibit the apoptosis of colon cancer cells and promote the proliferation of colon cancer cells (P < 0.05). The effect was significantly weakened when IL-22R1 was silenced (P < 0.05). Conclusion: IL-22R1 combined with IL-22 could promote the proliferation and inhibit apoptosis of colorectal cancer cells. In addition, blocking IL-22R1 could eliminate the influence of IL-22 on the proliferation and apoptosis of colorectal cancer cells.

The wild type gastrin receptor but not a colon cancer-derived gastrin receptor mutant mediates a pro-apoptotic effect of gastrin in colorectal cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A660-A661
Author(s):  
Frank Schmitz ◽  
Babette Reimann ◽  
Alexander Arlt ◽  
Karl H. Herzig ◽  
Wolfgang E. Schmidt ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Wild Type ◽  
Gastrin Receptor ◽  
Colorectal Cancer Cells ◽  
Apoptotic Effect ◽  
Receptor Mutant

Verbascoside Attenuates Rac-1 and HIF-1α Signaling Cascade in Colorectal Cancer Cells

2019 ◽  
Vol 18 (15) ◽  
pp. 2149-2155
Author(s):  
Danial Seyfi ◽  
Seyed B. Behzad ◽  
Mohammad Nabiuni ◽  
Kazem Parivar ◽  
Mohammad Tahmaseb ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Real Time ◽  
Real Time Pcr ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Ht29 Cells ◽  
Colorectal Cancer Cells

Objective: Metastasis phenotype is considered as the main challenge in colon cancer therapeutic methods. Furthermore, the side effects of conventional colorectal cancer treatment methods have attracted a lot of attention into natural ingredients. The aim of the study was to assess the molecular mechanism of verbascoside as natural bio-compound in human HT29 colon cancer cells. Methods: HT29 cells were cultured in RPMI-1640 medium containing 10% FBS and 1% penicillin/ streptomycin at 37°C and 5% CO2. HT-29 cells were treated with different concentrations of verbascoside (10, 20, 30, 40, 50, 70, 100 µg/ml) for 24 hours, then MTT assay was used to calculate 50% inhibitory concentration. The migration of the colon cancer cells was evaluated by scratch assay. To evaluate involved antiproliferative mechanism, Rac-1 (Ras-related C3 botulinum toxin substrate 1) and HIF-1α (hypoxia-inducible factor-1α) related gene expression were evaluated by Real Time PCR. Results: The results showed that verbascoside inhibited HT29 colon cancer cell proliferation dose-dependently and IC50 was evaluated as 50 μg/ml (***P<0.001). The results of wound healing assay demonstrated verbascoside decreased cell migration in a dose dependent manner. In the IC50 treated HT29 cells metastatic progression was significantly suppressed as **P<0.01. The results of Real Time PCR showed an attenuating effect of verbascoside on Rac-1, Zeb-1 (zinc finger E-box binding homeobox 1), Arp2 (Actin-Related Proteins), Pak1 (p21 (RAC1) activated kinase 1), VEGF (Vascular endothelial growth factor) and HIF-1α as Epithelial-Mesenchymal Transition markers. The down regulation of mRNA levels was Rac-1= 15.38, HIF-1 α = 16.66, Pak-1, Arp-2= 6.25, VEGF=24.39, Zeb-1=35.71 in HT29 cells treated with IC50 concentration of verbascoside. Conclusion: Colorectal cancer cells induce Rac-1 and HIF-1α overexpression which plays an important role in the activation and progression of cell motility, angiogenesis and metastasis. Overall results showed that verbascoside elucidated significant anti-metastatic and anti-invasion activities through suppression of Rac-1, HIF-1α, and Zeb-1 signaling pathway and it may be a suitable candidate to overwhelm colon cancer metastatic phenotype.

scholarly journals Cytotoxic Potential and Molecular Pathway Analysis of Silver Nanoparticles in Human Colon Cancer Cells HCT116

2018 ◽  
Vol 19 (8) ◽  
pp. 2269 ◽  
Author(s):  
Sangiliyandi Gurunathan ◽  
Muhammad Qasim ◽  
Chanhyeok Park ◽  
Hyunjin Yoo ◽  
Jin-Hoi Kim ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Dna Damage ◽  
Silver Nanoparticles ◽  
Cancer Cells ◽  
Ros Generation ◽  
Dead Cell ◽  
Colon Cancer Cells ◽  
Colorectal Cancer Cells

Silver nanoparticles (AgNPs) have gained attention for use in cancer therapy. In this study, AgNPs were biosynthesized using naringenin. We investigated the anti-colon cancer activities of biogenic AgNPs through transcriptome analysis using RNA sequencing, and the mechanisms of AgNPs in regulating colon cancer cell growth. The synthesized AgNPs were characterized using UV–visible spectroscopy (UV–vis), X-ray diffraction (XRD), Fourier-transform infrared spectroscopy (FTIR), dynamic light scattering (DLS), and transmission electron microscopy (TEM). The AgNPs were spherical with sizes of 2–10 nm. Cytotoxicity assays indicated that the AgNPs in HCT116 colorectal cancer cells were very effective at low concentrations. The viability and proliferation of colon cancer cells treated with 5 µg/mL biogenic AgNPs were reduced by 50%. Increased lactate dehydrogenase leakage (LDH), reactive oxygen species (ROS) generation, malondialdehyde (MDA), and decreased dead-cell protease activity and ATP generation were observed. This impaired mitochondrial function and DNA damage led to cell death. The AgNPs upregulated and downregulated the most highly ranked biological processes of oxidation–reduction and cell-cycle regulation, respectively. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that AgNPs upregulated GADD45G in the p53 pathway. Thus, the AgNP tumor suppressive effects were mediated by cell apoptosis following DNA damage, as well as by mitochondrial dysfunction and cell-cycle arrest following aberrant regulation of p53 effector proteins. It is of interest to mention that, to the best of our knowledge, this study is the first report demonstrating cellular responses and molecular pathways analysis of AgNPs in HCT116 colorectal cancer cells.

scholarly journals Enhancing cold atmospheric plasma treatment of cancer cells by static magnetic field

2016 ◽  
Vol 38 (1) ◽  
pp. 53-62 ◽  
Author(s):  
Xiaoqian Cheng ◽  
Kenan Rajjoub ◽  
Alexey Shashurin ◽  
Dayun Yan ◽  
Jonathan H. Sherman ◽  
...  
Keyword(s):  
Magnetic Field ◽  
Plasma Treatment ◽  
Cancer Cells ◽  
Static Magnetic Field ◽  
Atmospheric Plasma ◽  
Cold Atmospheric Plasma

scholarly journals Modifying Effects of Glucose and Insulin/Insulin-Like Growth Factors on Colon Cancer Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Şeyda Berk ◽  
Joseph A. M. J. L. Janssen ◽  
Peter M. van Koetsveld ◽  
Fadime Dogan ◽  
Naci Değerli ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Growth Factors ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Experimental Studies ◽  
Colon Cancer Cells ◽  
Colorectal Cancer Cells ◽  
Insulin Like Growth Factors

There are only a few experimental studies which have investigated effects of glucose alone, and glucose in combination with insulin/insulin-like growth factors (IGF) on the growth of colon cancer. In the present study, we studied in vitro in human colorectal cancer cells originating from four Dukes’ stages of colorectal cancer the effects of glucose, insulin and IGFs on proliferation, migration, cell cycle progression and gene expression of the IGF system. Growth of colon cancer cells originating from a Dukes’ stage A was glucose-dependent, whereas growth of cancer cells from Dukes’ stage B, C and D was glucose-independent. Stimulatory effects of insulin and IGFs on cell growth were observed only in colon cancer cells originating from Dukes’ stage C and D. IGF-II stimulated migration in Dukes’ stage B cells only. The growth stimulatory effects in Dukes’ stage C and D colorectal cancer cells were accompanied by G2/M arrest and associated with an increased IGF-IR/IGF-II receptor ratio. In conclusion, our in vitro data suggest that the stimulating effects of glucose, IGFs and insulin on proliferation differ between colorectal cancer cells from early and late Dukes’ stages. Stimulatory effects of glucose on proliferation appear predominantly present in stage Dukes’ stage A colorectal cancer cells, while in contrast growth factor-mediated stimulation of cell proliferation is more pronounced in Dukes’ late stage (metastasized) colorectal cancer cells. Moreover, our study suggests that a stringent glucose control may be important to control tumor growth in early stages of colorectal cancer, while inhibition of the endocrine actions of the IGFs and insulin become more important in the late (metastasized) stages of colorectal cancer to restrain growth of colon cancer cells.

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