Prostrate cells usually require testosterone and other androgens to survive. But some prostate cancer cells thrive despite treatments that eliminate androgens. One hypothesis is that estrogen, often considered a female hormone, may be activating genes normally controlled by androgen in these cancer cells. Describe one or more experiments to test this hypothesis. (See Figure 11.9 to review the action of these steroid hormones).

Short Answer

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The hypothesis stating the activation of prostate cancer cells is to check the interaction of estrogen hormones with receptors present within the nucleus. This interaction can activate the transcription of genes present in these cancer cells.

Step by step solution

01

Prostate cancer and its treatment 

Prostate cancer is male cancer that occurs in the prostate gland. The growth of this cancer takes place with the help of hormones such as testosterone.

The treatment for prostate cancer blocks testosterone. But in some cases, even the blockage of androgenic hormones makes the progress of cancer. This condition is due to the presence of estrogen hormones, a female hormone that helps the survival of the cancer cells.

02

Role of androgen and estrogen in prostate cancer 

The group of male hormones secreted in the body is known as androgen. Overproduction of androgen can result in prostate cancer. The other stimulant for the activation of prostate cancer is estrogen.

Estrogen is the female hormone with a similar role compared to the androgens in the activation of cancer cells.

03

Experiment to test the hypothesis that supports the survival of cancer cells.

The estrogen hormones present in the body interact with the receptor, leading to the formation of receptor hormone complex within the cell.

The hormone complex acts as a transcription factor that enters the nucleus and activates the gene present in the cancer cells. The transcription of a gene present in cancer helps in the survival of the prostate cancer cells.

The experiment can be framed to design an inhibitor that can bind to the cancer cell receptor. The inhibitor or ligand designed can block the transcription of the genes present in the cancer cells.

Thus, blocking the transcription process initiated by the receptor hormone complex can prove the hypothesis that estrogen can activate the genes present in cancer cells.

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Most popular questions from this chapter

Cell differentiation always involves

(A) transcription of the myoD gene.

(B) the movement of cells.

(C) the production of tissue-specific factors

(D) the selection loss of certain genes from the genome.

In general, what are the effects of histone acetylation and DNA methylation on gene expression?

The p53 protein can activate genes involved in apoptosis. Review Concept 11.5, and discuss how mutations in genes coding for proteins that function in apoptosis could contribute to cancer.

Once mRNA encoding a particular protein reaches the cytoplasm, what are four mechanisms that can regulate the amount of the protein that is active in the cell?

Trace amounts of dioxin were present in Agent Orange, a defoliant sprayed on vegetation during the Vietnam War. Animal tests suggest that dioxin can cause birth defects, cancer, liver and thymus damage, and immune system suppression, sometimes leading to death. But the animal tests are equivocal; a hamster is not affected by a dose that can kill a guinea pig. Dioxin acts like a steroid hormone, entering a cell and binding to a cytoplasmic receptor that then binds the cell’s DNA.

  1. Discuss how this mechanism might help explain the variety of dioxin’s effects on different body systems and in different animals.
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