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.

Insulin-like growth factors induce apoptosis as well as proliferation in LIM 1215 colon cancer cells

2007 ◽  
Vol 100 (1) ◽  
pp. 58-68 ◽  
Author(s):  
Ping Fu ◽  
Julian A. Thompson ◽  
Kerri S. Leeding ◽  
Leon A. Bach
Keyword(s):  
Colon Cancer ◽  
Growth Factors ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Insulin Like Growth Factors

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.

Activation by zinc of the human gastrin gene promoter in colon cancer cells in vitro and in vivo

Metallomics ◽  
2015 ◽  
Vol 7 (10) ◽  
pp. 1390-1398 ◽  
Author(s):  
Kathryn M. Marshall ◽  
Marie Laval ◽  
Ortis Estacio ◽  
Damien F. Hudson ◽  
Paul Kalitsis ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Growth Factors ◽  
Cancer Cells ◽  
Gene Promoter ◽  
Gastrointestinal Cancers ◽  
Colon Cancer Cells ◽  
Over Expression ◽  
Human Gastrin

Over-expression of growth factors can contribute to the development and progression of cancer, and gastrins in particular have been implicated in accelerating the development of gastrointestinal cancers.

scholarly journals Cell Cycle Arrest and Autophagy Induced by Compound Kushen Injection in sw620 and sw480 Colorectal Cancer Cells with p53 Mutation

2019 ◽  
Author(s):  
Jie Sun ◽  
Di Wang ◽  
Yu Zhang ◽  
Qing Mu ◽  
Mei Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Mutant P53 ◽  
Cycle Progression ◽  
Cycle Arrest ◽  
Colorectal Cancer Cells

Abstract Background Compound Kushen Injection (CKI) has been clinically used in China for 15 years to treat various types of solid tumors, including colorectal cancer. Here we examine cell cycle arrest, induced autophagy, and mutant p53 pathways perturbed by CKI in colorectal cancer cells. We and other groups have shown that CKI alters p53 gene expression patterns and suppresses proliferation in colorectal cancer cells. Methods We measured the effect of CKI on cell proliferation, cell cycle progression and autophagy in sw480 and sw620 colorectal cancer cells in vitro, and carcinogenesis and the progression of azoxymethane/dextran sodium sulfate-induced colorectal cancer in ICR mice in vivo. We also used RNA sequencing to analyze mRNA expression altered by CKI, and further validated the expression of mutant p53 and several genes in the cell cycle pathway using reverse transcriptase-quantitative PCR and western blotting. Using network pharmacology (BATMAN-TCM database), we have also predicted the active ingredients in CKI involved in regulating the expression of mutant p53. Results We show evidence that CKI significantly suppressed proliferation and cell cycle progression, and induced autophagy of sw480 and sw620 cells in vitro; it also inhibited the development of inflammatory colorectal cancer in vivo. We also show that the down-regulated expression of mutant p53 and adjustments in several key genes related closely to cell-cycle progression. Furthermore, N-oxysophocarpine, lupenone, and geranylacetone were predicted to be the active ingredients of CKI involved in the down-regulated expression of mutant p53. Conclusion Our results indicate that CKI likely acts as a potential anti-cancer therapeutic agent that targets the cell cycle pathway, suggesting a key role in the development of a novel subsidiary therapeutic approach against mutant p53 in patients with colorectal cancer.

scholarly journals Nrf3 Promotes 5-FU Resistance in Colorectal Cancer Cells via the NF-κB/BCL-2 Signaling Pathway In Vitro and In Vivo

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Bi-Qing Cai ◽  
Wan-Meng Chen ◽  
Jia Zhao ◽  
Wei Hou ◽  
Jian-Cai Tang
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Colon Cancer Cells ◽  
Tumor Drug Resistance ◽  
Colorectal Cancer Cells ◽  
Cancer Tissues ◽  
The Relationship

Increasing evidence indicates that nuclear factor, erythroid 2-like 3 (Nrf3) is connected with tumorigenesis. However, the relationship between Nrf3 and tumor drug resistance remains elusive. In this study, we investigated the effect and mechanism of action by which Nrf3 regulated the sensitivity of colon cancer cells to 5-fluorouracil (5-FU). We found Nrf3 was significantly increased in colon cancer tissues. Furthermore, we observed that Nrf3 knockdown and overexpression can significantly affect the sensitivity of colon cancer cells to 5-FU in vitro and in vivo. Moreover, Nrf3 promoted the expression of RELA, P-RELA, and BCL-2. Inhibition of NF-κB partly reversed the effects of Nrf3 overexpression, resulting in the resistance of colon cancer cells to 5-FU. Overall, the study revealed that Nrf3 was connected to the sensitivity of colon cancer cells to 5-FU, and its possible mechanism was related to the NF-κB signaling pathway, which provided a new target for overcoming the resistance of colon cancer cells to 5-FU.

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 Tumour-Derived Laminin α5 (LAMA5) Promotes Colorectal Liver Metastasis Growth, Branching Angiogenesis and Notch Pathway Inhibition

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 630 ◽  
Author(s):  
Alex Gordon-Weeks ◽  
Su Yin Lim ◽  
Arseniy Yuzhalin ◽  
Serena Lucotti ◽  
Jenny Adriana Francisca Vermeer ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Notch Pathway ◽  
Hepatic Metastases ◽  
Colon Cancer Cells ◽  
Vascular Basement Membrane ◽  
Colorectal Cancer Cells ◽  
Metastatic Growth ◽  
Metastasis Growth

Hepatic metastatic growth is dependent upon stromal factors including the matrisomal proteins that make up the extracellular matrix (ECM). Laminins are ECM glycoproteins with several functions relevant to tumour progression including angiogenesis. We investigated whether metastatic colon cancer cells produce the laminins required for vascular basement membrane assembly as a mechanism for the promotion of angiogenesis and liver metastasis growth. qPCR was performed using human-specific primers to laminin chains on RNA from orthotopic human colorectal liver metastases. Laminin α5 (LAMA5) expression was inhibited in colon cancer cells using shRNA. Notch pathway gene expression was determined in endothelia from hepatic metastases. Orthotopic hepatic metastases expressed human laminin chains α5, β1 and γ1 (laminin 511), all of which are required for vascular basement membrane assembly. The expression of Laminin 511 was associated with reduced survival in several independent colorectal cancer cohorts and angiogenesis signatures or vessel density significantly correlated with LAMA5 expression. Colorectal cancer cells in culture made little LAMA5, but its levels were increased by culture in a medium conditioned by tumour-derived CD11b+ myeloid cells through TNFα/NFκB pathway signalling. Down-regulation of LAMA5 in cancer cells impaired liver metastatic growth and resulted in reduced intra-tumoural vessel branching and increased the expression of Notch pathway genes in metastasis-derived endothelia. This data demonstrates a mechanism whereby tumour inflammation induces LAMA5 expression in colorectal cancer cells. LAMA5 is required for the successful growth of hepatic metastases where it promotes branching angiogenesis and modulates Notch signalling.

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