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Thesis (Ph.D) - University of Birmingham, Department of Medicine, Faculty of Medicine and Dentistry.
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Modulation of Apoptosis in Colon Cancer Cells by Bioactive Compounds. By Marinela Bostan, Mirela Mihaila, Camelia Hotnog, Coralia Bleotu, Gabriela Anton, Viviana Roman and Lorelei Irina Brasoveanu. Submitted: September 28th Reviewed: March 30th Published: September 7th Cited by: 1.
Title: Regulation of Apoptosis and Cell Survival by Resveratrol VOLUME: 7 ISSUE: 4 Author(s):Simone Fulda Affiliation:Institute for Experimental Cancer Research in Pediatrics, Goethe-University Frankfurt, Komturstrasse 3a, Frankfurt am Main, Germany. Keywords:Apoptosis, resveratrol, cancer Abstract: Tissue homeostasis is maintained by tight control of signaling events that regulate cell.
The pro-apoptotic proteins in the Bcl family have an opposing role in regulation of apoptosis and cell survival in colon cancer cells book regulation of apoptosis. Of the pro-apoptotic proteins, Bax and Bak were found to be involved in colonic expression obviously decreases in both the initiating and developmental stages in human CRC tis Bak was found to be able to prevent crypt hyperplasia by regulating spontaneous apoptosis Cited by: The JMJD2A demethylase regulates apoptosis and proliferation in colon cancer cells.
Apoptosis regulation: thus inhibiting carcinogenesis of human colon cancer cells. It has also been proposed that UVRAG is involved in causing membrane curving autophagy is induced for cell survival. Through autophagy, cells eliminate damaged organelles and may maintain their normal cellular function under adverse conditions of Cited by: 5.
The Role of Apoptosis in Cancer Therapy activate effector caspases or amplify the caspase cascades by increased activation of initiator caspases,13 Then the effector caspases cleave intracellular substrates, culminating in cell death,14Bcl-2 family members of proapoptotic and antiapoptotic proteins regulate.
Aberrant regulation of apoptotic cell death mechanisms is one of the hallmarks of cancer development and progression, and many cancer cells exhibit significant resistance to apoptosis signalling.
The results support the hypothesis that the two main species of ROS, superoxide and H 2 O 2, play different roles in cancer cell survival. The present work shows that HT induces apoptotic cell death and mitochondrial dysfunction by generating ROS in colon cancer cells.
Notably, REP1 is highly expressed in colon cancer tissues and cell lines, and silencing of REP1 sensitizes colon cancer cells to serum starvation- and 5-FU-induced apoptosis.
Wild-type p53 induces apoptosis in colon cancer cell lines. p53 mutations occur late in the adenoma-to-carcinoma sequence of colon cancer progression.
Gene silencing studies demonstrated that Bclsi-colon cancer cells (where the Bcl-2 gene has been inactivated by RNA interference techniques) induced pmediated apoptosis even in the. Colon cancer cells entering the liver through the hypoxemic portal circulation undergo massive cell death.
In order to cope with this metabolic stress, colon cancer cells induce the secretion of creatine kinase, brain-type (CKB) into the microenvironment by.
The adenomatous polyposis coli (APC) tumor suppressor is an essential negative regulator in the evolutionarily conserved Wnt/Wingless (Wg) signal transduction pathway. During normal development, Wnt signaling is required not only to induce cell proliferation and cell fate specification, but also to induce apoptotic cell death.
As anthocyanins have been described as mediators of apoptosis in different cancer cells, including non-small cell lung and colon cancer cells (Pal et al., ; Shin et al., ), the effect of. Selected Reviews: Degterev A, Yuan J () Expansion and evolution of cell death programmes. Nat. Rev. Mol. Cell Biol.
9(5), – Fuchs Y, Steller H () Programmed cell death in animal development and disease. Cell (4), –; Indran IR, Tufo G, Pervaiz S, Brenner C () Recent advances in apoptosis, mitochondria and drug resistance in cancer cells. PI3K/AKT regulation and an apoptosis discussion about some marine bioactive compounds on these aspects.
Cell Survival Survival Signaling via PI3K/AKT AKT plays an important role in cell survival . The PI3K/AKT pathway represents a key signal transduction pathway that mediates cell growth and blocks apoptosis . Keywords: Apoptosis, caspases, colon cancer cells, Luffa echinata Roxb For the treated cells, viability was calculated, p53 INTRODUCTION Colorectal cancer (CRC) is the third most common cancer in both males and females and the third leading cause of cancer death worldwide.[ 1 ].
It was observed that sanguinarine treatment induces a dose-dependent increase in apoptosis of human colon cancer cells. We also investigated the effects of sanguinarine on the expression of apoptosis-associated proteins, and the results revealed that there was an increase in Bax and a decrease in B-cell lymphoma 2 (Bcl-2) protein levels.
Several reports revealed that puerarin exerted an intriguing role in inducing cell apoptosis and suppressing cell proliferation especially in tumor cells. Apoptosis in colon cancer HT cells was. The abnormal apoptosis-autophagy cross talk helps cell death evasion.
First, the unusual autophagy proteins would result in apoptosis evasion. In normal apoptotic cells, autophagosome with the regulation of autophagy protein 9 (ATG9), ATG16L1, ATG5, and ATG12 shows a. Because ATF3 functions in regulation of cancer cell survival and apoptosis depending on tumor types, its function in HCC was still unclear.
Our data showed that downregulation of ATF3 expression level in HepG2 could remarkably abrogate effects of niclosamide on cell viability and activate caspase-3. Hartmann, Karin and Metcalfe, Dean D. () Regulation and dysregulation of mast cell survival and apoptosis.
In: Mast Cells and Basophils. San Diego, pp. 51. These events also commonly occurred in both cell lines, suggesting that fucoidan triggered G1 arrest and apoptosis in HCT cells by a pindependent mechanism. Thus, given that most tumors exhibit functional p53 inactivation, fucoidan could be a possible therapeutic option for cancer treatment regardless of the p53 status.
Caveolin-1 (CAV1) is an oncogenic membrane protein associated with endocytosis, extracellular matrix organisation, cholesterol distribution, cell migration and signaling.
Recent studies reveal that CAV1 is involved in metabolic alterations – a critical strategy adopted by cancer cells to their survival advantage. Consequently, research findings suggest that CAV1, which is altered in several.
Introduction. InKerr et al. described a distinct morphology of dying cells and called it apoptosis. The term was coined based on the fact that the release of apoptotic bodies by dying cells resembled the picture of falling leaves from deciduous trees, called in Greek “apoptosis”.This type of cell death has also been called programmed or physiological cell death, and is.
Apoptosis is a physiologically programmed cell death program that is also involved in defense mechanisms against damaged or stressed cells and cells stimulated by any agent to prevent the.
Deregulation of cell survival pathways and resistance to apoptosis are widely accepted to be fundamental aspects of tumorigenesis. As in many tumours, the aberrant growth and survival of colorectal tumour cells is dependent upon a small number of highly activated signalling pathways, the inhibition of which elicits potent growth inhibitory or apoptotic responses in tumour cells.
the two types of colon cancer cells are in discord. Transformation and transfection of ARK5 into the colorectal cancer cell line, HT did not prove beneficial. Similarly, glucosamine showed no clear pattern of reducing apoptosis in the cells.
Therefore, we propose further exploration of the inhibition of constitutive nitric. Anoikis Apoptosis Caspase Cell line Cell survival Colon Colorectal cancer DNA laddering Small intestine Regulated cell death This is a preview of subscription content, log in to check access.
Springer Nature is developing a new tool to find and evaluate Protocols. The prostate apoptosis response protein 4 (Par-4) is a tumor-suppressor that has been shown to induce cancer-cell selective apoptosis in a variety of cancers.
The regulation of Par-4 expression and activity is a relatively understudied area, and identifying novel.
We describe examples from fly and mouse model systems in which APC is required to prevent apoptosis, and thereby promote cell survival, during normal development.
Conversely, analysis of APC loss in cultured colonic carcinoma cells reveals that the resultant activation of β-catenin signaling promotes cell survival and inhibits cell death. VF reduced the cell viability and induced apoptosis in human colorectal cancer cells.
VF treatment increased both the protein and mRNA level of ATF3 and upregulated ATF3 promoter activity. The cis-element responsible for ATF3 transcriptional activation by VF was CREB which is located between [Formula: see text] to [Formula: see text]85 of.
was activated in CRC cells upon knockdown of LINC by annexin V and propidium iodide double staining via ﬂuores-cence-activated cell sorting (FACS) analysis,17 The results indi-cated that caspase-3 levels were increased in the siRNA-treated CRC cells, conﬁrming that LINC is involved in cell apoptosis (Figure 3C).
In addition, the apoptotic cell percentage was closely associated with down-regulation of Bcl-2 and up-regulation of Bax and caspase The results suggest that IOWE would be useful as an antitumor agent via the induction of apoptosis and inhibition of the growth of cancer cells through up-regulation of the expression of proapoptotic proteins.
Apoptosis, known as programmed cell death, is a carefully controlled, energy-dependent process of cell death. Induction of apoptosis results in a cascade of characteristic biochemical events resulting in changes in cellular morphology and death. Cells undergoing apoptosis display blebbing, cell shrinkage, nuclear fragmentation, and DNA.
Cellular changes should lead to activation of the apoptotic pathway and induction of cell death, which prevents tumor growth and progression. However, during tumorigenesis, some tumor cells develop apoptosis-resistant mechanisms that allow the cancer cells to avoid apoptotic cell death, resulting in the initiation and progression of human cancers.
In agreement with this hypothesis, down-regulation of miR expression could reverse the effect of ART on apoptosis of bladder cancer cells.
Young et al. reported that miR could bind the COX-2 3'-UTR and inhibit COX-2 expression in colorectal cancer cells. damaged cells and arrests the cell cycle. p53 is mutated or absent in some cancers and can not initiate apoptosis in malignant cells.
• Protein misfolding – unfolded protein response and ER stress – Alzheimer, Parkinson and Huntington diseases. • TNF Receptor family. • Cytotoxic T lymphocyte. Apoptosis can be triggered by various stimuli from outside or inside the cell, e.g.
by ligation of cell surface receptors, by DNA damage as a cause of defects in DNA repair mechanisms, treatment with cytotoxic drugs or irradiation, by a lack of survival signals, contradictory cell cycle signalling or by developmental death signals.
Growth Inhibition of Colon Cancer Cells is Due to Cell Cycle Arrest and Apoptotic Cell Death Based on the results reported in Figure 1 a, all the subsequent experiments were carried out in HT29 cells using µg GAE/mL for each fraction of the fruit (the dose that induced about 40–50% reduction in cell viability after 48 h treatment).
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potent inducer of apoptosis that may be a promising agent in cancer therapy due to its selectivity toward tumor cells. However, many cancer cells are resistant to TRAIL due to defects in apoptosis signaling or activation of survival pathways.
We hypothesized that a disruption of pro-survival signaling cascades with the multi. To get additional insights into the role of β-Catenin in the regulation of the cell cycle and apoptosis, we have analyzed the levels and subcellular localization of endogenous β-catenin and its relation with adenomatous polyposis coli (APC) during the cell cycle in S-phase–synchronized epithelial cells.
β-Catenin levels increase in S phase.defective apoptosis regulation is a fundamental aspect of the biology of cancer.
When it comes to the successful eradication of cancer cells by nonsurgical means, ultimately, all roads lead to apop-tosis. Essentially all cytotoxic anticancer drugs currently in clinical use, when they work, induce apoptosis of malignant cells.Knockdown of AKR1B10 significantly inhibited pinduced apoptosis in colorectal cancer cells, whereas the overexpression of AKR1B10 enhanced pinduced apoptosis and inhibited tumor proliferation in vivo.
Furthermore, low expression of AKR1B10 in colon cancer patients was correlated with decreased survival and poor prognosis.