BIOL 304 6380 What are the structure and function of cancer cells?

BIOL 304 6380 What are the structure and function of cancer cells?

BIOL 304 6380 What are the structure and function of cancer cells?

Discussion Topic 1:

In your own words, explain how cancer cells differ from normal cells regarding the following:

Telomeres, which are products of the telomerase enzyme

In cell division, telomeres are defined by the “end replication problem” of the DNA replication. After each round of DNA replication, each chromosome of a normal cell loses a short sequence of the telomere at its terminals (Noureen et al., 2021). However, in cancer cells, there is no loss of any DNA base pairs as the telomere maintains its length.

Cell-to-cell communication

Cancer cells communicated with each other to promote cancer metastasis and progression. However, the mechanism of communication is different from that of normal cells. For instance, normal cells communicate with each other by responding to signals from other cells whereas cancerous cells do not respond to signals from any other cell (Schwager et al., 2018).

Apoptosis

Apoptotic cell death is considered a normal part of the growth of normal cells and cannot be avoided. However, cancer cells have the potential of bypassing apoptosis in several ways with the p53 tumor suppressor gene that leads to loss of proapoptotic regulators being the most common (Aubrey et al., 2017).

Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response)

In normal cells, the Rb protein which is a tumor suppressor plays a significant role in tumor progression and

BIOL 304 6380 What are the structure and function of cancer cells
BIOL 304 6380 What are the structure and function of cancer cells

negative control of the cell cycle. Cdk and Cdk/cyclin complexes on the other hand lead to phosphorylation and CDKs activation which enables the progression of the cell cycle (Aubrey et al., 2017). p53 gene/protein on the other hand plays a significant role in cell division and cell death. However, in cancer cells, the p53 gene helps in promoting the growth and spread of cancer cells. Cdk and Cdk/cyclin complexes on the other hand inactivate the retinoblastoma protein pRb, causing the proliferation-associated E2F target genes subset expression.

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Discussion Topic 2:

In your own words, explain each of the hallmarks of cancer below:

  1. Immortality: Refers to the continuous cell division causing limitless replication. When normal cells uncontrollably continue to divide, with no intrinsic constraint, organs and tissues may develop to enormous sizes with health complications to the organisms (Hejmadi, 2014). Cancer cells have the capacity of dividing uncontrollably.
  2. Produce go signals: Most of the normal cells usually wait for a go signal for them to start dividing. However, cancer cells do not wait for a signal to start dividing, they rather produce their chemical signals to continue dividing (Hejmadi, 2014).
  3. Override stop signals: Normal cells usually stop diving when a stop signal is received (Hejmadi, 2014). Cancer cells do not respond to stop signals even from neighboring cells, they instead override these signals and keep on dividing.
  4. Resist cell death: In case of stress, normal cells may sometimes react accordingly by triggering a self-destruction signal and killing themselves (Hejmadi, 2014). Cancer cells on the other hand can avoid or sneak past such signals and continue dividing.
  5. Angiogenesis and how it relates to metastasis: For cancer cells to keep growing, they make sure that the sprouting of new blood vessels is stimulated to supply them with the required nutrients (Hejmadi, 2014).
  6. Metastasis: This is the spread of cancer cells to different body tissues and organs from their point of origin (Hejmadi, 2014).

To understand better strategies for cancer therapy, the hallmarks that address the progression of cancer at both cellular and molecular levels are considered important (Hejmadi, 2014). Such hallmarks include resisting cell death, overriding stop signal, and immortality. The others are also important as well.

References

Aubrey, B. J., Kelly, G. L., Janic, A., Herold, M. J., & Strasser, A. (2017). How does p53 induce apoptosis and how does this relate to p53-mediated tumor suppression? Cell Death & Differentiation25(1), 104–113. https://doi.org/10.1038/cdd.2017.169

Hejmadi M. (2014). Introduction to cancer biology (2nd ed.). Bookboon.com. Retrieved August 24 2022 from http://bookboon.com/en/introduction-to-cancer-biology-ebook.‌

Noureen, N., Wu, S., Lv, Y., Yang, J., Alfred Yung, W. K., Gelfond, J., Wang, X., Koul, D., Ludlow, A., & Zheng, S. (2021). Integrated analysis of telomerase enzymatic activity unravels an association with cancer stemness and proliferation. Nature Communications12(1), 139. https://doi.org/10.1038/s41467-020-20474-9

Schwager, S. C., Taufalele, P. V., & Reinhart-King, C. A. (2018). Cell–Cell Mechanical Communication in Cancer. Cellular and Molecular Bioengineering12(1), 1–14. https://doi.org/10.1007/s12195-018-00564-x