Scientific Literacy Essay

Squamous cell carcinoma is a form of skin cancer that occurs from continuous exposure of UV light to the skin. UV exposure poses a risk when people are not covered by clothing or any other proper protection, which is typically seen at places like the beach, where people forget to apply UV protectant sunscreen. The way ultraviolet light causes squamous cell carcinoma is by damaging the DNA inside skin cells, possibly altering how genes function. Our cells have ways of fixing damaged DNA, but not all damaged pieces are detected or repairable. The most common gene mutation that leads to squamous cell carcinoma is a mutation of the p53 gene. The beauty of the p53 gene is its ability to halt defective DNA that has been damaged or mutated from replicating. The mutation of the p53 gene therefore eliminates this function, allowing mutated DNA to replicate, possibly spreading mutant cells that develop into squamous cell carcinoma (Howell and Ramsey, 2023).

Collagen III, also known as type III collagen, is found in both connective tissues and organs just like many other collagens. collagen III is the composition of supportive structures for muscle cells, making it extremely important for the well-being of important organs like the heart. It works alongside collagen I, a stiff protein that has great tensile strength, while collagen III has a more elastic ability, giving it the power to store kinetic energy in the form of rebound. Collagen I also depends on collagen III to mature, with collagen I first building the scaffolding before collagen III comes in to finish it. Collagen III is also essential for wound healing but must be in the correct ratios with Collagen I to not create too thin tissues (Singh, Rai, and Agrawal, 2023).

Cancer and collagen III tie together during a unique phase of cancer’s lifespan, dormancy. Cancer cells tend to hide away in different organs after the primary tumor is removed, making them appear invisible to the observer. They lay dormant for a period of time, meaning they aren’t growth rapidly and causing chaos throughout the body, which makes people think they are free of cancer for good. The reality is that these secondary tumors are what kill majority of cancer patients, possibly because of how hard they are to track down once they enter dormancy. One piece of evidence for how cancer cells enter dormancy could lie in their relationship with collagen III. Research has found that cancer cells are able to utilize collagen III to create an extracellular matrix, essentially an anchor for tumor cells to latch onto host tissue and acts to regulate the tumor. The extracellular matrix (ECM) is in a way in charge of when a tumor goes from dormant to rapid growth. Current research has found that through manipulation of collagen III in keeping tumors dormant, there is a possibility of using this protein to slow tumor growth to a halt (Di Martino, Nobre, Mondal, Taha, Farias, Naba, Aguirre-Gisho, and Bravo-Cordero, 2021).

Dormant and proliferative cancer cells differ in how their extracellular matrix behaves. Dormant cancer cells have higher amounts of collagen III surrounding them, indicating that collagen III is particularly important to keeping cancer cells from proliferating. For dormant cancer cells to proliferate, a disturbance in the extracellular matrix must occur, meaning a disturbance in the collagen III content that keeps the cancer cells dormant in the first place. Both single cancer cells and metastasis have an extracellular matrix, but they behave in different ways. Single cancer cells have been found to have a more mesh-like extracellular matrix, while metastases have a linear extracellular matrix. It should also be said that dormant cancer cells have a mesh-like extracellular matrix, while proliferative cancer cells have a linear extracellular matrix, indicating that single cancer cells are typically dormant, while metastases are proliferative (Di Martino, Nobre, Mondal, Taha, Farias, Naba, Aguirre-Gisho, and Bravo-Cordero, 2021).

It is the way collagen III interacts with tumor cells that causes higher concentrations of collagen III to prevent tumor cells from proliferating. Collagen III has been found to have an inverse correlation with p-H3, an indicator of cells undergoing division, which explains why higher concentrations of collagen III are associated with lower or no growth of tumor cells. Another piece of evidence for this would be the analyzation of cancer cells when exposed to higher concentrations of collagen III. When exposed, almost all cancer cells have been found to be in the synthesis phase of interphase, with almost none found in G0/G1 or G2. G2 is associated with growth of cells, which would be seen in a proliferative tumor that was not being exposed to higher concentrations of collagen III. Single tumor cells are normally found in G0/G1, while metastases are found in all phases, as metastases are the proliferative kinds of cancer while the single tumor cells are typically the dormant kind. Being in G0/G1 for extended periods of time keeps single tumor cells as singular tumor cells. Cells must go from G0 to G2 for mitosis to occur in the first place, which explains how proliferative cancers can be observed in all phases throughout its mass (Di Martino, Nobre, Mondal, Taha, Farias, Naba, Aguirre-Gisho, and Bravo-Cordero, 2021).

Collagen III clearly has some effect on tumor cells that prevents them from growing and progressing into their proliferative stage. These effects can be seen at the single tumor cell level, where single tumor cells have more collagen III around them than proliferative metastases. As stated earlier, the single cells have a more mesh-like extracellular matrix and metastases have a more linear shaped extracellular matrix. These changes to the extracellular matrix can be attributed to the changes in collagen III levels seen around single tumor cells versus proliferative metastases. The dormant single tumor cells are smaller than proliferative metastases if that was not clear already. The levels of collagen III are inverse to the growth of tumor cells, as said before, which also means that the size of tumors should be inverse as well to the levels of collagen III surrounding the tumor. When tumors have been injected with collagen III, compared to a control without injection and to experiments with other collagens, the tumors injected with collagen III were the smallest. All this ties back to the basis of collagen III’s relationship with tumor cells, more collagen III is correlated with less tumor cell growth (Di Martino, Nobre, Mondal, Taha, Farias, Naba, Aguirre-Gisho, and Bravo-Cordero, 2021).

References

Howell, J., and Ramsey, M. (2023). Squamous Cell Skin Cancer. National Library of Medicine, https://www.ncbi.nlm.nih.gov/books/NBK441939/

Singh, D., Rai, V., and Agrawal, D. (2023). Regulation of Collagen I and Collagen III in Tissue Injury and Regeneration, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9912297/#:~:text=Collagen%20I%20is%20a%20stiff,distinct%20physical%20properties%20in%20nature

Di Martino, J., Nobre, A., Mondal, C., Taha, I., Farias, E., Fertig, E., Naba, A., Aguirre-Ghiso, J., Bravo-Cordero, J. (2021). A tumor-derived type III collagen-rich ECM niche regulates tumor cell dormancy, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8818089/#:~:text=ECM%20proteomics%20revealed%20that%20dormant,through%20DDR1%2Dmediated%20STAT1%20signaling