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Cellular Parabiosis

What is it?

Cellular parabiosis speaks to the ability of individual cells in tissue to share and exchange contents with each other: ions, small molecules, RNA, proteins and more. It provides “cellular solidarity” between cells, with one cell absent a particular molecule being “complemented” by another cell that has it. Cellular parabiosis appears to be important in maintaining healthy cells, including preventing cancer, but paradoxically, once it breaks down and cancer emerges, also appears to be important in driving tumour growth and survival.

How is cellular parabiosis enabled?

Via transport vehicles such as exosomes, pores such as gap junctions, and intercellular networks through structures such as “tunneling nanotubes” (TNTs) and “tumour microtubes” (TMs).

Where does cellular parabiosis happen?

Examples includes many normal “syncytial” tissues: muscle cells, cardiac myocytes, neurons and others. Cellular parabiosis appears to be essential in the maintenance of healthy cells and tissues, including the prevention of cancer. Indeed, there is evidence that it is the disruption of normal cellular parabiosis, for example through inflammation, that allows cancers to develop.

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The role of cellular parabiosis in established cancer

However, in established cancer Friend turns enemy: Primary tumours establish their own “unhealthy” cellular networks that help the cancer cells survive and grow. Additionally these networks may also enable cancer cells to resist chemotherapy and radiotherapy through various mechanisms.

Large malignant cellular networks have been observed in glioblastoma, where cancer cells make direct anatomical connections between cells through structures terms tumour microtubes, ultra-long membrane protusions that the tumour uses for brain invasion, proliferation, and interconnection over long distances. These networks also protect glioblastoma cells from radiotherapy and chemotherapy.

 

 

 

CELLULAR REFERENCES
MacKenzie, Ian, and Peyton Rous. “The experimental disclosure of latent neoplastic changes in tarred skin.” The Journal of Experimental Medicine 73, no. 3 (February 28, 1941): 391–416.
MacKenzie, Ian, and Peyton Rous. “The experimental disclosure of latent neoplastic changes in tarred skin.” The Journal of Experimental Medicine 73, no. 3 (February 28, 1941): 391–416.
Rous, Peyton, and John G. Kidd. “Conditional neoplasms and subthreshold neoplastic states.” The Journal of Experimental Medicine 73, no. 3 (February 28, 1941): 365–90.
Berenblum, I., and P. Shubik. “The Role of Croton Oil Applications, Associated with a Single Painting of a Carcinogen, in Tumour Induction of the Mouse’s Skin.” British Journal of Cancer 1, no. 4 (December 1947): 379–82.
Murray, A. W., and D. J. Fitzgerald. “Tumor Promoters Inhibit Metabolic Cooperation in Cocultures of Epidermal and 3T3 Cells.” Biochemical and Biophysical Research Communications 91, no. 2 (November 28, 1979): 395–401.
Stoker, M. G. P., Moira Shearer, and C. O’neill. “Growth Inhibition of Polyoma-Transformed Cells by Contact with Static Normal Fibroblasts.” Journal of Cell Science 1, no. 3 (September 1, 1966): 297–310.
McCullough, K. D., W. B. Coleman, G. J. Smith, and J. W. Grishan. “Age-Dependent Regulation of the Tumorigenic Potential of Neoplastically Transformed Rat Liver Epithelial Cells by the Liver Microenvironment.” Cancer Research 54, no. 14 (July 15, 1994): 3668–71.