Cancer cells have been known to use sagacious methods of evading apoptosis and mysteriously overcoming powerful anti-cancer therapies. One such method of evasion has recently been identified as the process of epithelial-mesenchymal transition (EMT) and its reverse process, mesenchymal-epithelial transition (MET). These transitions enable epithelial cells (structural/fixed) to gain mesenchymal cell (differentiating/mobile) functions, and vice versa. Researchers believe that epithelial-mesenchymal plasticity (EMP) allows cancers to become therapy resistant, determines cancer aggressiveness and allows metastatic cancer to mobilize and spread.
“Such dynamic and reversible switching can help tumor cells to overcome various challenges during disease progression such as anoikis, and assaults by the immune system.”
These processes and their characterization in cancer have been studied, however, questions remain about their molecular determinants and degree of reversibility, or irreversibility, in different cell populations and environments. To further elucidate EMT, researchers from Rice University, Northeastern University and the Indian Institute of Science used mechanistic mathematical models to identify possible mechanisms that may drive EMT response to an EMT-inducing signal in a given isogenic cell population. Their paper was published by Oncotarget in 2020, and entitled, “Epigenetic feedback and stochastic partitioning during cell division can drive resistance to EMT.”
Full blog - https://www.oncotarget.org/2021/10/21/emt-resistance-in-cancer-cells-and-two-potential-causes/
Press release - https://www.oncotarget.com/news/pr/epigenetic-feedback-and-stochastic-partitioning-can-drive-resistance-to-emt/
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DOI - https://doi.org/10.18632/oncotarget.27651
Full text - https://www.oncotarget.com/article/27651/text/
Correspondence to - Herbert Levine - h.levine@northeastern.edu and Mohit Kumar Jolly - mkjolly@iisc.ac.in
Keywords - epithelial-mesenchymal transition, mesenchymal-epithelial transition, GRHL2, epigenetics, asymmetric cell division
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