Isothiocyanates are compounds found in vegetables such as broccoli. Such compounds have been shown to induce the expression of proteins called caspases in cervical cancer cells. Outside of Cell Toxins TNF DNA Damage p63 Bd-2 Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of broccoli to promote, suppress or have no effect on the progression or survival of cervical cancer cells? Promote progression of cervical cancer cells Suppress progression of cervical cancer cells Have no effect on progression of cervical cancer cells

Isothiocyanates are compounds found in vegetables such as broccoli. Such compounds have been shown to induce the expression of proteins called caspases in cervical cancer cells. Outside of Cell Toxins TNF DNA Damage p63 Bd-2 Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of broccoli to promote, suppress or have no effect on the progression or survival of cervical cancer cells? Promote progression of cervical cancer cells Suppress progression of cervical cancer cells Have no effect on progression of cervical cancer cells

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter32: The Reception And Transmission Of Extracellular Information

Section: Chapter Questions

Problem 21P

See similar textbooks

Similar questions

Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.
Cancer-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.
The P63 and P53 have similar functionalities in the cell, however, p53 is rarely associated directly with p63, suggesting that p63 may indirectly act as an oncogene by blocking p53 function. This hypothesis may also explain why p63 is associated with other indications of misinterpretation. I do understand the above statement, however once piece not clear – why would p63 block p53 function? Have these genes been shown to have opposing functions? From the background information provided above, it seems like they would have seminar functions. Explain.
TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival as shown in the graph below. Which of the following would you observe in these cells treated with TNF- alpha? Select all that apply TNF-a 120 100 80 - 60- 40- 20 - 24 72 (hrs) + Control - TNF-a 10ng + TNF-a 100 ng O Activation of extrinsic pathway of apoptosis O Activation of intrinsic pathway of apoptosis Activation of executioner caspases Recruitment of adapter protein FADD to the TNF-alpha receptor LNCAP cell viability (% of control)
''In the cellular regulatory pathways that controlcell growth and proliferation, the products of oncogenesare stimulatory components and the products of tumorsuppressor genes are inhibitory components.'' 'Is this statement true? Explain why or why not.
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!
One important role of Fas and Fas ligand is to medi-ate the elimination of tumor cells by killer lymphocytes.In a study of 35 primary lung and colon tumors, half thetumors were found to have amplified and overexpressed agene for a secreted protein that binds to Fas ligand. How doyou suppose that overexpression of this protein might con-tribute to the survival of these tumor cells? Explain yourreasoning.
Under normal physiological conditions, proto-oncogenes and tumor suppressorshelp control cell growth and proliferation. When mutated, these proteinscontribute to the development of cancer. Briefly detail the molecular basis of thisphenomenon
Explain why mutations in tumor suppressor genes are recessive (both copies of the gene must be defective for the regulation of cell division to be defective), whereas mutations in oncogenes are dominant.
BCL2 binds to and inactivates BAX and other pro-apoptotic proteins, thereby inhibiting apoptosis. Venetoclax has been approved for marketing in patients with chronic lymphocytic leukemia (CLL) Venetoclax is a highly selective BCL2 inhibitor that disrupts the interaction of this protein with BH3 domain proteins thereby permitting apoptosis. Proapoptotic Proapoptotic proteins protein binds to BCL2 BCL2 Venetoclax Venetoclax displaces proapoptotic proteins BCL2 Venetoclax Proapoptotic proteins No venetoclax binding BCL2 Glys01Val mutation Which of the following can you conclude from this information? Select all that apply Bcl2- mutations that prevent Ventoclax binding promote cell survival Venetoclax binding to Bcl2 promotes cell survival . Venetoclax binding to Bcl2 promotes cell death Proapoptotic protein binding to Bcl2 promotes cell survival
Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.
a. A typical cellular response of a mammary epithelial cell to EGF signal is proliferation. the Kd for the interaction between EGF and its receptor is 1x10^-10 M. Lets imagine that at least 25% of the receptors on a normal cell must be engaged by EGD in order to trigger the cellular proliferation response. What minimum concentration of EGF is required to reduce cell proliferation? (Show calculation). b. Mammary epithelial cancer cells have amplified levels of EGF receptors on their surface. If such a cell has 1000 EGF receptors, as compared to 200 receptors on a normal cell, what minimum concentration of EGF is required to induce cell proliferation in the cancer cell? [Show calculation]. Note that the same number of receptors (not percentage of receptors) must be activated to promote proliferation in normal cells and cancer cell. c. The ambient (unstimulated) concentration of EGF in mammary epithelial tissue is 1x10^-11 M. Will this level of EGF stimulate proliferation in normal…