Biochemistry: The Molecular Basis of Life
6th Edition
ISBN: 9780190209896
Author: Trudy McKee, James R. McKee
Publisher: Oxford University Press
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Chapter 16, Problem 5Q
Summary Introduction
To review:
The possible consequences of phorbol esters in an initiated cell and the enzymes activated by phorbol esters and DAG.
Introduction:
Cancer is a multistage process and it initiates with initiating events usually viral infection or exposure to a carcinogen. These initial events are then followed by contact with tumor promoters. Tumor promoters are chemical molecules that activate cell proliferation; however, they do not have the ability to initiate the formation of a tumor on their own.
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Cancer often results from a multistage process involving an initiating event (mediated by a viral infection or a carcinogenic chemical), followed by exposure to tumor promoters. Tumor promoters, a group of molecules that stimulate cell proliferation, cannot induce tumor formation by themselves. The phorbol esters, found in croton oil (obtained from the seeds of the croton plant, Croton tiglium), are potent tumor promoters. (Other examples of tumor promoters include asbestos and several components of tobacco smoke.) In one of the tumor-promoting actions of the phorbol esters, these molecules mimic the actions of DAG. In contrast to DAG, the phorbol esters are not easily disposed of. Explain the possible biochemical consequences of phorbol esters in an “initiated” cell. What enzyme is activated by both DAG and phorbol esters?
The deregulation of several signal transduction pathways is integral to the onset of
cancer. These pathways involve both tumor promoters (the "gas pedals") and tumor
suppressors (the "brake pedals").
Which would be a more effective treatment for cancer: A small molecule inhibitor
that targets a tumor suppressor or one that targets a tumor promoter? Briefly
explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND
MINIMALLY IN ABOUT EIGHT WORDS.)
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The p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.
Chapter 16 Solutions
Biochemistry: The Molecular Basis of Life
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Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biochemistry and related others by exploring similar questions and additional content below.Similar questions
- The Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!arrow_forward"In the cellular regulatory pathways that control cell growth and proliferation, the products of oncogenes are stimulatory components and the products of tumor suppressor genes are inhibitory components" is true or false.arrow_forwardduring tumor progression, additional mutations occur within multiple cells of a tumor population, leading to multiple different clones of cells within that tumor. Some) but not all) clones may eventually metastasize, depending on the number and type of mutations that occur in those clones. true falsearrow_forward
- p53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). Armed with your knowledge about the different mechanisms which govern transcription and translation, what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?arrow_forwardCancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.arrow_forwardTumor-suppressor genes are normal human genes that prevent uncontrollable cell growth. Starting with a normal laboratory humancell line, describe how you could use transposon tagging to identifytumor-suppressor genes. (Note: When a TE hops into a tumorsuppressorgene, it may cause uncontrolled cell growth. This is detected as a large clump of cells among a normal monolayer of cells.)arrow_forward
- The p53 gene is a tumor-suppressor gene while p634 gene is an oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.arrow_forwardStudies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?arrow_forwardp53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?arrow_forward
- Tumor suppressor proteins can assist in slowing down the cell cycle under appropriate conditions. In humans, the TP53 gene encodes a tumor suppressor called p53. Most mutations in the TP53 gene result in a mutant form of p53 that can no longer function to slow down the cell cycle, which can lead to a cell becoming cancerous. However, some mutant forms of p53 actually possess the ability to increase a cell's resistance to anticancer treatments. Which of the following BEST describes the latter type of mutation? loss-of-function mutation gain-of-function mutation suppressor mutation reverse mutationarrow_forwardCancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.arrow_forwardMetastasis occurs when cells from a primary tumor invade and colonize other tissues. Metastasis is a complex, multistep process. Tumor cells must lose adhesion with other tumor cells, invade local tissues and vessels, move through the circulation, leave the vessels, and finally, establish new colonies at distant sites. Tumor cells gain the ability to cross epithelial layers and migrate through tissues by mutations, although the nature of the mutations that drive metastasis is poorly understood. Mutations that block expression of the E-cadherin gene are thought to be an important step in metastasis. The absence of E-cadherin expression could affect metastasis by blocking cell adhesion directly, by releasing signaling proteins bound to the cytoplasmic domain of E-cadherin, or by both mechanisms. To better understand how loss of E-cadherin contributes to metastasis, scientists created two cell lines that differed in their expression of E-cadherin. One cell line was blocked for expression…arrow_forward
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