Cell adhesion intimately linked to metabolism?

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Discussion Overview

The discussion centers around the potential link between cell adhesion and metabolism, particularly in the context of cancer and mechanobiology. Participants explore the implications of this relationship for research and therapeutic applications, including stem cell therapy and cancer metastasis.

Discussion Character

  • Exploratory
  • Technical explanation
  • Debate/contested

Main Points Raised

  • Some participants note the established role of integrin-PI3K-Akt signaling in metabolism but express difficulty in finding research that directly links cell adhesion to metabolic processes.
  • One participant suggests that if cell adhesion is compromised, it could lead to metabolic shutdown as a protective mechanism against cancer metastasis.
  • Another participant mentions the concept of mechanobiology and its influence on cell behavior, including morphology and gene transcription, but finds a lack of specific studies connecting cell adhesion to metabolism regulation.
  • A participant raises concerns about the efficacy of stem cell therapies, suggesting that cells in suspension may be predisposed to metabolic arrest before injection, potentially leading to poor outcomes.
  • One reply challenges the idea that the body can selectively shut down a specific cell's metabolism, emphasizing that cellular responses are based on local effects rather than organismal control.
  • Another participant references existing research on mechanosensation and tissue dynamics, particularly in bone remodeling and kidney repair, while noting that the relationship between cell-matrix adhesion and the cell cycle is still not fully understood.
  • One participant mentions ongoing research by Donald Ingber's lab on cell adhesion and mechanosignaling in cancer, suggesting potential therapeutic avenues, though this research is still in early stages.
  • A participant recalls integrin's association with insulin receptors and growth factors, hinting at possible connections to metabolic pathways.

Areas of Agreement / Disagreement

Participants express a range of views on the relationship between cell adhesion and metabolism, with no consensus reached. Some acknowledge the complexity of the topic and the need for further research to clarify these connections.

Contextual Notes

Participants highlight limitations in existing research, including a lack of direct studies linking cell adhesion to metabolism and the complexity of translating cellular behaviors to organismal effects.

gravenewworld
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Integrin-PI3K-Akt signal transduction is well known. Akt signaling has been heavily reviewed and is well known to play a role in metabolism. So why do I have difficulty finding any research that has linked cell adhesion to metabolism? It would make sense. If a cell became cancerous, one way for the body to protect against metastasis would be to shut down the metabolism of that cell if its adhesion started to go haywire in order to prevent it from spreading. I could see profound effects on research here if a clear link between cell adhesion and metabolism were ever made. Anyone know of any papers on this It would also be interesting in a sense that something purely mechanical, like cell adhesion, could control metabolism.
 
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Trying looking up mechanobiology, there is a tonne of research out there regarding the effect substrate material properties (stiffness, topography, friction etc) adjust cell behaviour.
 
Ryan_m_b said:
Trying looking up mechanobiology, there is a tonne of research out there regarding the effect substrate material properties (stiffness, topography, friction etc) adjust cell behaviour.
I have, the only thing I can find ( and that we were taught) is that mechanobiology regulates morphology, transcription of certain genes, differentiation, etc., but I can not find anything specifically linking cellular adhesion to regulation of metabolism. I've done quick searches on integrins and metabolism, integrin and metabolism regulation, etc. but come up with nothing decent.
 
Also it would make sense then that many stem cell therapy trials end up failing or produce mediocre results (which is what we are observing for the most part) if people are just making suspensions of stem cells and trying to simply inject them in praying for a clinical effect. If the cells are in suspension before being injected they could already be primed for failure before the experiment even really begins if they're on the path towards metabolic arrest no?
 
gravenewworld said:
Integrin-PI3K-Akt signal transduction is well known. Akt signaling has been heavily reviewed and is well known to play a role in metabolism. So why do I have difficulty finding any research that has linked cell adhesion to metabolism? It would make sense. If a cell became cancerous, one way for the body to protect against metastasis would be to shut down the metabolism of that cell if its adhesion started to go haywire in order to prevent it from spreading. I could see profound effects on research here if a clear link between cell adhesion and metabolism were ever made. Anyone know of any papers on this It would also be interesting in a sense that something purely mechanical, like cell adhesion, could control metabolism.

I think you are mixing up a few concepts- for example 'the body' cannot not shut down a particular cell except as an immune response. Cells act based on *local* effects, and 'metabolism' is an organismal concept- going from the cell to the organism isn't fully understood yet.

The only work I know of linking mechanosensation and tissue dynamics is in the context of either bone remodeling or stem cells. Even so, there is a clear relation between cell-matrix adhesion and the cell cycle- for example, injury repair. In the kidney, the epithelial cells de-differentiate, proliferate to restore tubule integrity, and then re-differentiate. The hypothesis is that flow sensing drives this process, but the details are still unknown. (shameless self-promotion: I have a recent PLOS article showing that mechanical stimulation changes the differentiation process in renal epithelia)

Another link is in cancer metastasis: cells detach from the matrix, migrate to the blood, and then travel throughout the body. It is known that secondary tumors are not formed randomly: IIRC, prostate cancer preferentially seeds in the bone. This process is not understood, and is sometimes the "soil or the seed" problem.

http://www.regonline.com/builder/site/tab1.aspx?EventID=1032604
 
I'm not sure about metabolism, but a lot of labs, such as the laboratory of Donald Ingber at Harvard, have studied the role of cell adhesion and mechanosignalling in cancer development. See for example http://www.sciencedirect.com/science/article/pii/S1535610805002679. Furthermore, it has been proposed that tissue engineering strategies could possibly be used to convert cancerous cells back to normal cells although this research is only in the early stages: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570051/
 
I remember integrin being associated with insulin receptors and growth factor.
 

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