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Most cancer-busting strategies focus on removing cancerous cells. While this approach has proved extremely effective on many patients, most treatments have unpleasant side effects and there are many strains which prove extremely challenging to remove. An alternative model to this is to alter instead of remove – fixing cancerous behaviour by ‘reprogramming’ cells that go rogue; essentially swiss finishing school for cellular miscreants. A study published in Nature Cell Biology now provides hope that this tactic could in fact work in many cancers.
Researchers from Mayo Clinic’s Florida campus have found that adhesion proteins, which act like a glue sticking cells together, actually interact with a cell’s ‘microprocessor’. This processor creates molecules called miRNAs, which regulate multiple genes and essentially activate or de-activate different behavioural programs (like commands in computer programming). When healthy cells bump into a neighbour and begin to glue together, these adhesion proteins normally influence both cells – tuning down growth pathways. In cancer, the lab found this adhesion is perturbed; de-regulating miRNA production and enabling rampant growth. When scientists corrected these miRNA levels, the growth was arrested.
“The study brings together two so-far unrelated research fields — cell-to-cell adhesion and miRNA biology — to resolve a long-standing problem about the role of adhesion proteins in cell behavior that was baffling scientists. Most significantly, it uncovers a new strategy for cancer therapy”
In the video below, Panos Anastasiadis, Ph.D., from Mayo Clinic’s Florida campus comments on the findings:
While this approach might not be applicable to every type of cancer and wouldn’t reverse mutations, it could provide another way of limiting aggressive expansion and steering cells back to a non-threatening state, also rendering them easier to remove.
By administering the affected miRNAs in cancer cells to restore their normal levels, we should be able to re-establish the brakes and restore normal cell function’
Read more at NeuroscienceNews
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