Answered: Based on the data provided, explain how…

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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The SIRT3 protein has been reported to increase the growth of certain types of cancer cells. Researchers studying the metabolism and development of stomach cancer cells investigated the potential role of the SIRT3 protein in these cells. In the first investigation, the researchers quantified the relative amount of SIRT3 in normal stomach cells and in each of four different lines of stomach cancer cells (Figure 1). Using data from a group of 100 patients with stomach cancer, the researchers also analyzed the relative amount of SIRT3 protein detected in samples of the cancer cells and in normal cells immediately adjacent to the cancer cells (Figure 2).

Figure 1. SIRT3 protein levels in normal stomach cells (NS) and stomach cancer cell lines from four different patients (SC-1, SC-2, SC-3, SC-4), shown relative to the level in normal stomach cells (NS). Error bars represent ±SEx¯.

Figure 2. The number of patients, from 100 tested, whose stomach cancer cells or normal stomach cells adjacent to the cancer cells express high, low, or no SIRT3 protein

In the second investigation, the researchers grew four groups of stomach cells in petri dishes containing nutrient broth:• NS, normal stomach cells• SC-1, a line of stomach cancer cells that the researchers had examined for SIRT3 expression• SC+RNA, the SC-1 line of stomach cancer cells to which a plasmid was added that encodes a small RNAcomplementary to a portion of the SIRT3 mRNA. When these small RNAs bind to the complementary portion of SIRT3 mRNA, the SIRT3 mRNA is broken down rather than translated.• SC+plasmid, the SC-1 line of stomach cancer cells to which a plasmid was added that does NOT encode the complementary small RNA
After 24 hours of growth, the researchers measured several indicators of metabolism by an equal number of all four cell groups: glucose uptake, lactic acid production, and the level of cytoplasmic ATP production in the presence of a compound that blocks the electron transport chain (Figure 3). The values were calculated relative to the values obtained for normal stomach cells.
Figure 3. Glucose uptake, lactic acid production, and cytoplasmic ATP levels in stomach cells. NS, normal stomach cells; SC-1, stomach cancer cells; SC+ plasmid, SC-1 cells with added plasmid only; SC+RNA, SC-1 cells with added plasmid encoding small RNAcomplementary to a portion of SIRT3. Error bars represent ±SEx¯.

(d) Based on the data provided, explain how cellular processes must be altered in stomach cancer cells compared with normal stomach cells to result in the different levels of SIRT3 expression observed. A mutation to the gene encoding a cyclin-dependent kinase (CDK) in human stomach cells results in a CDK that is continually active in the cells. Explain why the continually active CDK will most likely change the normal cells into cancer cells.

The SIRT3 protein has been reported to increase the growth of certain types of cancer cells. Researchers studying the metabolism and development of stomach cancer cells investigated the potential role of the SIRT3 protein in these cells. In the first investigation, the researchers quantified the relative amount of SIRT3 in
normal stomach cells and in each of four different lines of stomach cancer cells (Figure 1). Using data from a group of 100 patients with stomach cancer, the researchers also analyzed the relative amount of SIRT3 protein detected in samples of the cancer cells and in normal cells immediately adjacent to the cancer cells
(Figure 2).
111
NS SC-1 SC-2 SC-3 SC-4
Figure 1. SIRT3 protein levels in normal stomach cells (NS) and stomach cancer cell lines from four different patients (SC-1, SC-2, SC-3, SC-4), shown relative to the level in normal stomach cells (NS). Error bars represent +SET.
Number of Patients
100
80
60
40
20-
2.5-
2.0
1.5-
1.0
0
0.0
Normal
Stomach
Cells
2.0
Figure 2. The number of patients, from 100 tested, whose stomach cancer cells or normal stomach cells adjacent to the cancer cells express high, low, or no SIRT3 protein
●
In the second investigation, the researchers grew four groups of stomach cells in petri dishes containing nutrient broth: NS, normal stomach cells SC-1, a line of stomach cancer cells that the researchers had examined for SIRT3 expression SC + RNA, the SC-1 line of stomach cancer cells to which a plasmid was
added that encodes a small RNA complementary to a portion of the SIRT3 mRNA. When these small RNAs bind to the complementary portion of SIRT3 mRNA, the SIRT3 mRNA is broken down rather than translated.• SC + plasmid, the SC-1 line of stomach cancer cells to which a plasmid was added that does
NOT encode the complementary small RNA
• After 24 hours of growth, the researchers measured several indicators of metabolism by an equal number of all four cell groups: glucose uptake, lactic acid production, and the level of cytoplasmic ATP production in the presence of a compound that blocks the electron transport chain (Figure 3). The values were
calculated relative to the values obtained for normal stomach cells.
1.6-
1.2
0.8
0.4-
0.0
Stomach
Cancer
Cells
NS
High SIRT3 expression
Low SIRT3 expression
No SIRT3 expression
SC-1
SC+Plasmid
Glucose uptake
Lactic acid production
Cytoplasmic ATP level
SC+RNA
• Figure 3. Glucose uptake, lactic acid production, and cytoplasmic ATP levels in stomach cells. NS, normal stomach cells; SC-1, stomach cancer cells; SC+ plasmid, SC-1 cells with added plasmid only; SC + RNA, SC-1 cells with added plasmid encoding small RNA complementary to a portion of SIRT3. Error
represent +SET.

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