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Cell Biology Final Assignment Background More than one in ten women develop breast cancer during life, but death rates have declined steadily because of earlier detection and new treatments. As with other forms of cancer , breast cancer results from mutations in DNA. When enough mutations accumulate, a cell can be more readily triggered to reproduce by division and ignore signals that trigger death by apoptosis . This rapidly dividing cell forms a tumor, which differs in structure and function from normal tissue. Ultimately, some of these cells leave the tumor and enter the bloodstream. Death results when these cells circulate to vital organs and interfere with their functions. Scientists have identified a signaling pathway called the GPR/TRPV signaling pathway that regulates reproduction and death of cells in breast tissue (Figure 1). In the absence of the signaling molecule S1 (Figure 1, left panel), the receptor GPR is in its inactive form. The subsequent structures: G- complex, Erk1, and p38, are also in their inactive form, thus cell division does not occur. Similarly, TRPV is in its inactive form in the absence of S1. Consequently, the concentration of calcium ions (Ca 2+ ) does not increase and the structures ATM and p53 are in their inactive form, thus cell death does not occur. When S1 is present (Figure 1, right panel), the following steps occur: GPR signaling pathway 1) A signal called S1 binds to the receptor GPR, inducing a conformational change. 2) The active form of GPR binds and phosphorylates the G-complex. 3) The active form of the G-complex binds and phosphorylates a kinase called Erk1. 4) The activation of Erk1 leads to the activation of a kinase called p38 by phosphorylation. 5) The activation of p38 leads to an increase in cell division. TRPV signaling pathway

1) A signal called S1 binds to the receptor TRPV, preventing a conformational change. 2) The inactive form of TRPV does NOT open a channel to allow Ca 2+ to move into the cell. 3) Since Ca 2+ levels in the cell do NOT increase, a kinase called ATM can NOT become activated by phosphorylation. 4) Since ATM is NOT activated, this does NOT lead to the activation of p53 by phosphorylation. 5) Since p53 is NOT activated, this does not lead to an increase in cell death by apoptosis. Figure 1. The GPR/TRPV signaling pathway that regulates cell division and cell death of cells found in breast tissue. Left: When no signaling molecule (S1) is present, all proteins and processes in the signaling pathway are inactive and [Ca 2+ ] in the cell do not increase. Right: When the signaling molecule S1 is present, it binds to the receptor GPR, inducing a conformational change. The activation of GPR results in the phosphorylation of the proteins/structures downstream of GPR - specifically the G-complex, Erk1, and p38, ultimately resulting in an increase in cell division. Additionally, when the signaling molecule S1 is present, it binds to the receptor TRPV, preventing a conformational change. The inactivation of TRPV means that Ca 2+ does not flow into the cell and thus the [Ca 2+ ] inside the cell does not increase. Consequently, ATM and p53 are not

phosphorylated, thus no cell death by apoptosis occurs. Designing an effective treatment for breast cancer requires an understanding of the signaling pathways that determine whether cells reproduce or die, such as the GPR/TRPV signaling pathway (Figure 1). Researchers discover effective treatments through experiments, testing each molecule to determine to what extent that molecule disrupts the function of signaling pathways responsible for inducing cancer as well as the mechanisms by which a given treatment works. Scenario You work for a drug company that aims to develop a new treatment for breast cancer. Previously, scientists discovered that people with breast cancer have unusually high concentrations of endocannabinoids . Researchers at your company hypothesized that endocannabinoids interfere with the GPR/TRPV signaling pathway that controls cell division and cell death in the cells of breast tissue. However, the exact mechanisms remain unclear. If you can determine the mechanism by which endocannabinoids stimulate cell division and inhibit cell death, you can identify potential treatments that would treat breast cancer. To complete this assignment, you should follow the sequence of steps below: Step 1: Determine if receptor(s) in the GPR/TRPV signaling pathway bind to endocannabinoids. Step 2: Determine how the presence of endocannabinoids affects the activity of downstream proteins in the cytoplasm of the GPR/TRPV signaling pathway. Step 3: Evaluate potential treatments for breast cancer. Step 1: Determine if receptor(s) in the GPR/TRPV signaling pathway bind to endocannabinoids.

Before we can start exploring potential cancer treatments, we will explore how (if at all) the presence of endocannabinoids affects the GPR/TRPV signaling pathway. We’ll start by determining if the receptor(s) in the GPR/TRPV signaling pathway bind to endocannabinoids and, if so, the impact of this binding on the activity of the receptors GPR and TRPV. The following experiment was conducted. Ten genetically identical cells were collected from healthy breast tissue. The relative activity (% of observed max) of the receptors GPR and TRPV were separately measured in these healthy cells. Then, the cells were exposed to an endocannabinoid suspected to be associated with causing breast cancer (called ENDO1) and the measurements were repeated. Using this information, answer the following questions. Part 1 - Effect of endocannabinoids on the activity of GPR Directions : For questions 1-5, download the “Act III: The Cure Workbook” from your Canvas assignment and refer to the sheets titled “Question 1” and “Q2-5 Effect of ENDO1 on GPR.” These sheets contain the activity (%) of GPR in the absence or presence of endocannabinoids (sample size = 10 activities per category, absence or presence of ENDO1). Use Excel for calculations, modeling, and graphing. 1. Use the sheet (tab) labeled “Question 1” to create a plot of a linear relationship between the categorical independent variable (absence or presence of ENDO1) and the activity of GPR. Your plot should follow the formatting guidelines listed below. Formatting Instructions General ● Chart type: Line with Markers ● Quick layout: Layout 4 ● Chart title: “Activity of GPR in response to ENDO1” ● Y-axis title: “Mean relative activity of GPR (%)”; Font size = 32 ● Y-axis numbers: Font size = 24 ● X-axis title: “Absence or presence of ENDO1”; Font size 32 ● X-axis numbers: Font size = 24 ● Line: No line Marker ● Marker options: Built in, Filled in circle, Size = 10

● Fill: Solid fill, Color = Black ● Border: Solid line, Color = Black Error bars → Standard deviation ● Direction: Both ● End style: Cap ● Error amount: Custom → Select the appropriate cell in Excel. ● Line: Solid line ● Color: Black ● Width: 2 pt Y-axis ● Bounds: minimum at 0, maximum at 100 ● Units: Major = 10, Minor = 5 2. Based on the figure that you made in Question 1 describe how the absence or presence of ENDO1 affects the activity of GPR. In other words, how does the activity of GPR in the absence of ENDO1 compare to the activity of GPR in the presence of ENDO1? After formulating a cart in excel on the data of absence or presence of ENDO1, it is obvious that the GPR is much more active in the presence of ENDO1 than in the absence. 3. Estimate the standard deviation of the linear relationship between the categorical independent variable (absence or presence of ENDO1) and the activity of GPR. Round all calculated values to the nearest tenth of a decimal place. For example, if you calculate the value as 5.252%, you would round your answer to 5.3%. Standard deviation = 1.3 4. Estimate the mean activity of GPR in the absence of ENDO1. Round all calculated values to the nearest tenth of a decimal place. For example, if you calculate the value as 5.252%, you would round your answer to 5.3%. Mean activity = 7.3

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