scholarly journals Pathway Analysis of Fucoidan Activity Using a Yeast Gene Deletion Library Screen

Marine Drugs ◽  
2019 ◽  
Vol 17 (1) ◽  
pp. 54 ◽  
Author(s):  
Monika Corban ◽  
Mark Ambrose ◽  
Joanne Pagnon ◽  
Damien Stringer ◽  
Sam Karpiniec ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cancer Cells ◽  
Gene Deletion ◽  
Undaria Pinnatifida ◽  
Colon Cancer Cells ◽  
Cellular Processes ◽  
Anti Cancer ◽  
Library Screen ◽  
Deletion Library

Fucoidan, the sulfated fucose-rich polysaccharide derived from brown macroalgae, was reported to display some anti-cancer effects in in vitro and in vivo models that included apoptosis and cell cycle arrest. The proposed mechanisms of action involve enhanced immune surveillance and direct pro-apoptotic effects via the activation of cell signaling pathways that remain largely uncharacterized. This study aimed to identify cellular pathways influenced by fucoidan using an unbiased genetic approach to generate additional insights into the anti-cancer effects of fucoidan. Drug–gene interactions of Undaria pinnatifida fucoidan were assessed by a systematic screen of the entire set of 4,733 halpoid Saccharomyces cerevsiae gene deletion strains. Some of the findings were confirmed using cell cycle analysis and DNA damage detection in non-immortalized human dermal fibroblasts and colon cancer cells. The yeast deletion library screen and subsequent pathway and interactome analysis identified global effects of fucoidan on a wide range of eukaryotic cellular processes, including RNA metabolism, protein synthesis, sorting, targeting and transport, carbohydrate metabolism, mitochondrial maintenance, cell cycle regulation, and DNA damage repair-related pathways. Fucoidan also reduced clonogenic survival, induced DNA damage and G1-arrest in colon cancer cells, while these effects were not observed in non-immortalized human fibroblasts. Our results demonstrate global effects of fucoidan in diverse cellular processes in eukaryotic cells and further our understanding about the inhibitory effect of Undaria pinnatifida fucoidan on the growth of human cancer cells.

α-Mangostin induces G1 cell cycle arrest in HCT116 cells through p38MAPK-p16INK4a pathway

RSC Advances ◽  
2015 ◽  
Vol 5 (44) ◽  
pp. 34752-34760 ◽  
Author(s):  
Sovannarith Korm ◽  
Ho-Chang Jeong ◽  
Ok-Seon Kwon ◽  
Jeong-Rak Park ◽  
Hyeseong Cho ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Garcinia Mangostana ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
G1 Cell Cycle Arrest ◽  
Active Substances ◽  
Hct116 Cells

α-Mangostin (α-MG), one of the active substances inGarcinia mangostana, has been shown to exhibit anti-cancer effects in HCT116 colon cancer cells.

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 GHRH antagonist causes DNA damage leading to p21 mediated cell cycle arrest and apoptosis in human colon cancer cells

Cell Cycle ◽  
2009 ◽  
Vol 8 (19) ◽  
pp. 3149-3156 ◽  
Author(s):  
Florian Hohla ◽  
Stefan Buchholz ◽  
Andrew V Schally ◽  
Stefan Seitz ◽  
Ferenc G. Rick ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Cycle Arrest ◽  
Human Colon Cancer Cells

Argentatin B derivatives induce cell cycle arrest and DNA damage in human colon cancer cells through p73/p53 regulation

2017 ◽  
Vol 27 (3) ◽  
pp. 834-843 ◽  
Author(s):  
Juan Carlos Romero-Benavides ◽  
Natalia Bailon-Moscoso ◽  
Hortensia Parra-Delgado ◽  
Maria Isabel Ramirez ◽  
Javier Villacis ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Induce Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Human Colon Cancer Cells

scholarly journals Apelin Effects Migration and Invasion Abilities of Colon Cancer Cells

Cells ◽  
2018 ◽  
Vol 7 (8) ◽  
pp. 113 ◽  
Author(s):  
Marta Podgórska ◽  
Katarzyna Pietraszek-Gremplewicz ◽  
Dorota Nowak
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Development ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Cellular Processes ◽  
Anti Cancer ◽  
Cancer Types ◽  
Membrane Type

Colon cancer is one of the most common cancer types. Its positive correlation with general obesity has led to increasing amounts of research focusing on the role of adipokines in colon cancer development. Apelin is a peptide released by adipose tissue that could affect many cellular processes connected with carcinogenesis. In this study, we examined the role of apelin in the motility regulation of colon cancer cells. We showed that the effect of four different apelin peptides increased the ability of cancer cells to migrate and invade examined cells trough influencing migratory protrusions formation and actin cytoskeleton rearrangement. Additionally, using confocal microscopy, we noticed that apelin stimulated the proteolytic activity of cancer cells, especially increasing the level of membrane-type 1 matrix metalloprotease. Taken together, apelin increased the movement of colon cancer cells through several possible mechanisms. Moreover, better understanding the process through which apelin regulates cancer development is still necessary to the creation of novel anti-cancer therapy.

Cancer Treatment with Liposomes Based Drugs and Genes Co-delivery Systems

2018 ◽  
Vol 25 (28) ◽  
pp. 3319-3332 ◽  
Author(s):  
Chuanmin Zhang ◽  
Shubiao Zhang ◽  
Defu Zhi ◽  
Jingnan Cui
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Synergistic Effects ◽  
Resistance Mechanisms ◽  
Delivery Systems ◽  
Cell Cycle Checkpoints ◽  
Drug Efflux ◽  
Cancer Resistance ◽  
Cancer Models ◽  
Anti Cancer

There are several mechanisms by which cancer cells develop resistance to treatments, including increasing anti-apoptosis, increasing drug efflux, inducing angiogenesis, enhancing DNA repair and altering cell cycle checkpoints. The drugs are hard to reach curative effects due to these resistance mechanisms. It has been suggested that liposomes based co-delivery systems, which can deliver drugs and genes to the same tumor cells and exhibit synergistic anti-cancer effects, could be used to overcome the resistance of cancer cells. As the co-delivery systems could simultaneously block two or more pathways, this might promote the death of cancer cells by sensitizing cells to death stimuli. This article provides a brief review on the liposomes based co-delivery systems to overcome cancer resistance by the synergistic effects of drugs and genes. Particularly, the synergistic effects of combinatorial anticancer drugs and genes in various cancer models employing multifunctional liposomes based co-delivery systems have been discussed. This review also gives new insights into the challenges of liposomes based co-delivery systems in the field of cancer therapy, by which we hope to provide some suggestions on the development of liposomes based co-delivery systems.

scholarly journals Pro-Apoptotic Activity of Artichoke Leaf Extracts in Human HT-29 and RKO Colon Cancer Cells

2021 ◽  
Vol 18 (8) ◽  
pp. 4166
Author(s):  
Milena Villarini ◽  
Mattia Acito ◽  
Raffaella di Vito ◽  
Samuele Vannini ◽  
Luca Dominici ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Chlorogenic Acid ◽  
Cancer Cells ◽  
Herbaceous Plant ◽  
Colon Cancer Cells ◽  
Leaf Extracts ◽  
Caffeoylquinic Acids ◽  
Induction Of Apoptosis ◽  
Ht 29

(1) Background: Cynara cardunculus L. subsp. scolymus (L.) Hegi, popularly known as artichoke, is an herbaceous plant belonging to the Asteraceae family. Artichoke leaf extracts (ALEs) have been widely used in traditional medicine because of their hepatoprotective, cholagogic, hypoglycaemic, hypolipemic and antibacterial properties. ALEs are also recognized for their antioxidative and anti-inflammatory activities. In this study, we evaluated the cytotoxic, genotoxic, and apoptotic activities, as well as effect on cell growth of ALEs on human colon cancer HT-29 and RKO cells. HT-29 and RKO cells exhibit a different p53 status: RKO cells express the wild-type protein, whereas HT-29 cells express a p53-R273H contact mutant. (2) Methods: Four different ALEs were obtained by sequential extraction of dried artichoke leaves; ALEs were characterized for their content in chlorogenic acid, cynaropicrin, and caffeoylquinic acids. HT-29 and RKO cells were used for in vitro testing (i.e., cytotoxicity and genotoxicity assessment, cell cycle analysis, apoptosis induction). (3) Results: Two out of the four tested ALEs showed marked effects on cell vitality toward HT-29 and RKO tumour cells. The effect was accompanied by a genotoxic activity exerted at a non-cytotoxic concentrations, by a significant perturbation of cell cycle (i.e., with increase of cells in the sub-G1 phase), and by the induction of apoptosis. (4) Conclusions: ALEs rich in cynaropicrin, caffeoylquinic acids, and chlorogenic acid showed to be capable of affecting HT-29 and RKO colon cancer cells by inducing favourable biological effects: cell cycle perturbation, activation of mitochondrial dependent pathway of apoptosis, and the induction of genotoxic effects probably mediated by the induction of apoptosis. Taken together, these results weigh in favour of a potential cancer chemotherapeutic activity of ALEs.

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